Prove an interpretation?

[Nesslig20]

I will make a reply on the rest of your post within a few days.

Probably going to be the same question, Again and again and again.....and again.

That comment is irrelevant since Behes concern has nothing to do with common ancestry, as far as I know Behe accepts common ancestry, his only concern is that according to him Darwinian mechanisms (mutations and natural selection) cant account for the diversity and complexity of life that we have.

You mentioned Irreducible complexity, as if it wasn't disproved, which it is for more then 10 years now!. And now you are pretending that this has nothing to do with Behe, which it obviously does.

He does indeed accept common ancestry, however he is still wrong with irreducible complexity. He has been shown to be wrong and I have shown you to be wrong with the citations I provide that you still are trying to ignore.

the comment is also a straw man because those who deny common ancestry do not claim that the similarities between humans and other species are a product of chance.

It is not "just similarities" as I have explained before, but again, you have short term memory. It is the pattern of both the presence of similarities or common traits and the absence of them, the differences. And this pattern forms a twin nested hierarchy (an evolutionary tree) that taxonomy revealed a hundred years before Darwin was alive and just become more robust over time.

But this get conclusive with genetics. Just like we can calculate, based on a paternity test, that the probability (or better yet, the certainty) of the child being that of the father (or not) is 99% Thus practically certain that he is the father.

The certainty of all life related is >99,999999999999999999999999999999999999999999999999999...etc

And the certainty that humans are related to other species is >99,999999999999999999999999999999999999999999999999999999999999999
9999999999999999999999999999999999999999999999999999999999999999999999999999999999999999999999999999999999999999999
999999999999999999999999999999999999999999999999999999999999999999999999999999999999999999999....etc

And that is just from genetics alone and no competing hypothesis that explains why we even have common genetic markers with other life forms that form the same twin nested hierarchy. Design doesn't predict this, just like design doesn't predict that two unrelated people would be tested as 99% certain to have a parental relationship on a paternity test.

"Unless the designer made it such to give the illusion that all life is related just to test our faith."

But common design DOES predict this.

But why cant I simply use the anthropic principle (multiverse theory for example) to explain that probability? .............if we wouldn't have 97% similarities with chimps we wouldn't be wondering why chimps and humans have a 97% similarity. ..........in other words observers that ask this question can only exist in universes where chimps and humans have a 97% similarity.

Now you are just rambling nonsense. The anthropic principle relates to either of these two things.
1. Humans require a specific environment within the universe to live.
2. Humans require a specific universe (with specific physical properties) to exists.

How the fuck are either of these related to genetics at all??

And we don't just say that we are related with chimps just because we are 97% similar genetically, though that is a strong indication, but it wasn't the definitive factor. It is shared genetic markers that we have: orthologs, ERVs, shared pseudogenes (how does design explain that). Fusion of chromosome number 2, which was predicted by common descent.

I am not accusing you in particular, but many atheist (Dawkins for example) use the anthropic principle to get away with the probabilities that theist provide, so why cant I do the same?..........this is really an honest question, I really what to know about your thoughts on the anthropic principle and on weather if we should use it or not to explain away probabilistic problems.

Because you have no idea what those things even are. You are literally saying something absurd like this.
"If fishermen can use a rod catching fish, why can't I use a rod to fix my car?"

 

[leroy]

:Mutations that change a necessary function a gene would be harmful if there was only one of it, but duplications negate this harmful effect, thereby allowing the copy to freely mutate without any harm to the organism.
This has (at least) two implications. The copy can change its function to fulfill a novel role which is beneficial. Of course this is an indirect benefit of a mutation that creates the potential for some future mutation to be beneficial (which would still count as beneficial). But this alone would probably not be enough, so what direct benefits has. It creates redundancy. Organisms that have many duplicated forms of their genes don't suffer from the harmful effects of mutations as much.

Those mutations by definition are neutral, redundant mutation are neutral..............I could grand that in the long term (after adding other mutations) the effect could be positive, this is the neutralist view, but the fact is that if an individual has a gene duplication it wont be selected by natural selection unless it has a benefit, natural selection doesn't have a mind, natural selection wont have a bias in keeping a mutation just because the mutation has potencial long term benefits.

the fact is that the probability of fixation of a neutral mutation (even if it has long term benefits) is 1/2N

N = size of the populaton

so even in a small population of 1000 individuales, the probability of fixation is 1/2,000...............this is why we know that in the majority of cases a specific neutral mutation will be removed by genetic drift. .....the only way to reduce this probability is if the mutation has a benefit. and this is why adding to many neutral mutations would produce a probabilistic problem.


So please answer this question, any objection that I might have depends on how you answer this question.

talking about the evolution of sight...........are you a neutralist or a selectionist?


Neutralist> you believe that most mutations, (related to the evolution of sight) where neutral and selected by random genetic drift

Selectionists>, Most mutations (related to the evolution of sight) where positive and selected by natural selection.

 

[leroy]

It is not "just similarities" as I have explained before, but again, you have short term memory. It is the pattern of both the presence of similarities or common traits and the absence of them, the differences. And this pattern forms a twin nested hierarchy (an evolutionary tree) that taxonomy revealed a hundred years before Darwin was alive and just become more robust over time. ......

yes, and all I am saying is that those who deny common ancestry, don't argue that the pattern was a product of chance, therefore any probabilistic arguments are irrelevant. and strawman.

Now you are just rambling nonsense. The anthropic principle relates to either of these two things.
1. Humans require a specific environment within the universe to live.
2. Humans require a specific universe (with specific physical properties) to exists.

How the fuck are either of these related to genetics at all??

And we don't just say that we are related with chimps just because we are 97% similar genetically, though that is a strong indication, but it wasn't the definitive factor. It is shared genetic markers that we have: orthologs, ERVs, shared pseudogenes (how does design explain that). Fusion of chromosome number 2, which was predicted by common descent.

How about this answer....

We live in a multiverse, with a potentially infinite number of universes, in most of these universes humans and chimps, don't have all these shared ERVs pseudogenes, proteins.....etc......but in a small minority of these multiverses just by chance, we happen to have all this shared stuff with chimps. We simply happen to live in such universe, if we weren't living in such universe we wouldn't be wondering why we have all this shared stuff and similarities with chimps.


Obviously this is a stupid answer, but my point is that some atheist use the same kind of answer to explain away some theistic arguments, why cant we simply reject those atheists answers for the same reason you would reject my answer?


this is really an honest question, I don't have any hidden motives, I honestly what to know about your thoughts

 

[Rumraket]

Obviously this is a stupid answer, but my point is that some atheist use the same kind of answer to explain away some theistic arguments, why cant we simply reject those atheists answers for the same reason you would reject my answer?

We can, I absolutely agree, reject such an answer as completely idiotic and unsatisfying. One can basically explain away everything with that kind of "answer".

Some atheistic arguments, or responses, are in fact stupid and silly. I have no compunction agreeing to that. I'm an atheist yet it is entirely obvious to me that some atheists are atheists for bad reasons, or have no, or bad answers to some theistic arguments. In becoming an atheist, one does not magically transform into some sort of flawless logic-computer that only make correct arguments.

 

[Rumraket]

:Mutations that change a necessary function a gene would be harmful if there was only one of it, but duplications negate this harmful effect, thereby allowing the copy to freely mutate without any harm to the organism.
This has (at least) two implications. The copy can change its function to fulfill a novel role which is beneficial. Of course this is an indirect benefit of a mutation that creates the potential for some future mutation to be beneficial (which would still count as beneficial). But this alone would probably not be enough, so what direct benefits has. It creates redundancy. Organisms that have many duplicated forms of their genes don't suffer from the harmful effects of mutations as much.

Those mutations by definition are neutral, redundant mutation are neutral..............I could grand that in the long term (after adding other mutations) the effect could be positive, this is the neutralist view, but the fact is that if an individual has a gene duplication it wont be selected by natural selection unless it has a benefit, natural selection doesn't have a mind, natural selection wont have a bias in keeping a mutation just because the mutation has potencial long term benefits.

the fact is that the probability of fixation of a neutral mutation (even if it has long term benefits) is 1/2N

N = size of the populaton

so even in a small population of 1000 individuales, the probability of fixation is 1/2,000...............this is why we know that in the majority of cases a specific neutral mutation will be removed by genetic drift.

Yes. So what? In the majority of cases. Key word there is majority. Not all. Majority.

You seem to be somehow trying to conclude that, if the mutation is neutral, it won't fix at all (this is basically what you want to get to). You seem to be trying to get at that conclusion so that you can say that the eye could not evolve if it involved steps that required neutral mutations.

Again, we know of situations with REQUIRED neutral mutations fixing in populations with BILLIONS of individuals. Some times fixing before the next mutation happened that was beneficial. Some times hovering around at a low frequency (meaning it hadn't fixed yet) before the next mutation happened, which in conjunction with the neutral one, was benficial. For example, the evolution of chloroquine resistance in the Malaria parasite Plasmodium Falciparum, requires at least one neutral mutation to evolve before additional beneficial mutations can happen. To get at the highest levels of chloroquine resistance requires some times three to four neutral, or even deleterious mutations.

Here look at this:

The blue horizontal arrows are neutral mutations. The green ones are beneficial, the red are deleterious. The Y-axis denotes levels of resistance. Notice how, to even get ANY resistance to chloroquine, neutral mutations have to happen first. Only in conjunction with the +75E, or +76T mutations, both of which are neutral, can chloroquine resistance even arise. Then several additional beneficial ones become possible, but to get even higher from those, the route again involves neutral or even deleterious steps. Steps observed having evolved in nature, in real Plasmodium populations.
Source of the figure:
Summers, R. L., Dave, A., Dolstra, T. J., Bellanca, S., Marchetti, R. V., Nash, M. N., Richards, S. N., Goh, V., Schenk, R. L., Stein, W. D., Kirk, K., Sanchez, C. P., Lanzer, M. and Martin, R. (2014) Diverse mutational pathways converge on saturable chloroquine transport via the malaria parasite’s chloroquine resistance transporter. Proceedings of the National Academy of Sciences. published online April 11, 2014. [doi: 10.1073/pnas.1322965111]


So your desired conclusion simply doesn't follow. The fixation probability is low, but it's not zero, nor is it "borderline infinitesimal". Or "so low as to be virtually identical to zero and so we can basically dismiss it". Are you somehow trying to say that events with a probability of 1 in 1000, or 1 in 50.000, or 1 in 1 million, never take place? That would be idiotic, because that's obviously not what a probability means. A probability of occurrence is a RATE of occurence. It means it actually occurs, as opposed to not at all occurring.

You need to make your argument more explicit instead of this sort of trying to handwave it away with "the odds are sorta low". Yes, they are, but it could still happen (and has been observed happening), so you can't reject evolution for that reason alone.

 

[Deleted member 619]

Some atheistic arguments, or responses, are in fact stupid and silly. I have no compunction agreeing to that. I'm an atheist yet it is entirely obvious to me that some atheists are atheists for bad reasons, or have no, or bad answers to some theistic arguments. In becoming an atheist, one does not magically transform into some sort of flawless logic-computer that only make correct arguments.

This.

In fact, these days, I spend far more effort in correcting these bad arguments than I do arguing with theists.

 

[surreptitious57]

I agree with this. Those on our side know you re one of the best when it comes to identifying flaws in argumentation. So are only too happy
to learn from you. Whereas those on the other side have no such obligation. I think it more psychologically satisfying from your perspective
because some are actually paying attention to what you are saying. Though having said that it would not surprise me if you also had some
from the other side given the popularity of the blog. Especially as the most read post was one on evolution. So keep up with the good work

 

[Deleted member 619]

That's very kind of you, mate.

 

[Nesslig20]

:Mutations that change a necessary function a gene would be harmful if there was only one of it, but duplications negate this harmful effect, thereby allowing the copy to freely mutate without any harm to the organism.
This has (at least) two implications. The copy can change its function to fulfill a novel role which is beneficial. Of course this is an indirect benefit of a mutation that creates the potential for some future mutation to be beneficial (which would still count as beneficial). But this alone would probably not be enough, so what direct benefits has. It creates redundancy. Organisms that have many duplicated forms of their genes don't suffer from the harmful effects of mutations as much.

Those mutations by definition are neutral

No they are not, and I explained that in that very quote that I highlighted. It has one benefit creating genetic redundancy. I also mentioned right next to this quote genetic dosage, meaning duplication can have an EFFECT that can be beneficial, thus NOT neutral.

A mutation that occurs within one organism that has only one copy of each gene would be more likely to be harmful compared to a mutation that occurs with an organism that has many copies of each gene. There are many duplications that have been lost as a result of being redundant, we have 49 duplicated Cytochrome C pseudogenes for example.
Another way is that duplication provide gene dosage which amplifies the effect of a gene (which may or may not be beneficial), thus duplications can be favored if increase in gene dosage is beneficial.

Thus duplications are beneficial (in many different ways) and thus provide a clear advantage that can be favored by natural selection.

, redundant mutation are neutral..............

No, I didn't say redundant mutation, I said duplications that create redundancy, which can be beneficial. I have shown you peer reviewed articles (copy pasted) to you.

Loss of Genetic Redundancy in Reductive Genome Evolution[/url]"]Biological systems evolved to be functionally robust in uncertain environments, but also highly adaptable. Such robustness is partly achieved by genetic redundancy, where the failure of a specific component through mutation or environmental challenge can be compensated by duplicate components capable of performing, to a limited extent, the same function. Highly variable environments require very robust systems. Conversely, predictable environments should not place a high selective value on robustness. Here we test this hypothesis by investigating the evolutionary dynamics of genetic redundancy in extremely reduced genomes, found mostly in intracellular parasites and endosymbionts. By combining data analysis with simulations of genome evolution we show that in the extensive gene loss suffered by reduced genomes there is a selective drive to keep the diversity of protein families while sacrificing paralogy. We show that this is not a by-product of the known drivers of genome reduction and that there is very limited convergence to a common core of families, indicating that the repertoire of protein families in reduced genomes is the result of historical contingency and niche-specific adaptations. We propose that our observations reflect a loss of genetic redundancy due to a decreased selection for robustness in a predictable environment.

Evolution of genetic redundancy[/url]"]Genetic redundancy means that two or more genes are performing the same function and that inactivation of one of these genes has little or no effect on the biological phenotype. Redundancy seems to be widespread in genomes of higher organisms1, 2, 3, 4, 5, 6, 7, 8, 9. Examples of apparently redundant genes come from numerous studies of developmental biology10, 11, 12, 13, 14, 15, immunology16,17, neurobiology18,19 and the cell cycle20,21. Yet there is a problem: genes encoding functional proteins must be under selection pressure. If a gene was truly redundant then it would not be protected against the accumulation of deleterious mutations. A widespread view is therefore that such redundancy cannot be evolutionarily stable. Here we develop a simple genetic model to analyse selection pressures acting on redundant genes. We present four cases that can explain why genetic redundancy is common. In three cases, redundancy is even evolutionarily stable. Our theory provides a framework for exploring the evolution of genetic organization.

I could grand that in the long term (after adding other mutations) the effect could be positive,

That is called potentiating mutation. A mutation that leads to the potential for another mutation to have a beneficial effect. Of course in this case, duplications can be both potentiating and beneficial.

this is the neutralist view, but the fact is that if an individual has a gene duplication it wont be selected by natural selection unless it has a benefit, natural selection doesn't have a mind, natural selection wont have a bias in keeping a mutation just because the mutation has potencial long term benefits.

Of course, I have shown to you the benefits. But will ignore that anyway. If potentiating mutation don't have a benefit, they can be fixed in the population by GENETIC DRIFT!! Which does happen.

the fact is that the probability of fixation of a neutral mutation (even if it has long term benefits) is 1/2N
N = size of the populaton
so even in a small population of 1000 individuales, the probability of fixation is 1/2,000...............this is why we know that in the majority of cases a specific neutral mutation will be removed by genetic drift. .....the only way to reduce this probability is if the mutation has a benefit. and this is why adding to many neutral mutations would produce a probabilistic problem.

Humans have 49 Cytochrome pseudogenes as a result of many duplication events. What is the chance? The reason why is because so many duplications happen, it is CERTAIN that some will be inherited just by genetic drift alone. The same is with all mutations. There are so many mutations that are largely neutral that it is guaranteed that some of them will spread or even get fixed in the population. That is why we have variations among individuals that don't seem to be of any benefit. If you are or your family members have blond hair and blue eyes or red heads, those traits have no benefits.

"That a particular specified event or coincidence will occur is very unlikely. That some astonishing unspecified events will occur is certain. That is why remarkable coincidences are noted in hindsight, not predicted with foresight."
—David G. Myers

So please answer this question, any objection that I might have depends on how you answer this question.
talking about the evolution of sight...........are you a neutralist or a selectionist?

Both. Since there are so many neutral mutation (some that do lead to changes in phenotypes) that get inherited, genetic drift has been proven to be a larger role in the evolution of species. Does that mean natural selection played no role? No, it still does.

Neutralist> you believe that most mutations, (related to the evolution of sight) where neutral and selected by random genetic drift
Selectionists>, Most mutations (related to the evolution of sight) where positive and selected by natural selection.

[/quote]

Both, there probably were many neutral mutations that are involved in the evolution of eyes (duplication among of them, although duplications CAN also be beneficial) and there were indeed mutations that had a selective benefit for better sight.

It is not "just similarities" as I have explained before, but again, you have short term memory. It is the pattern of both the presence of similarities or common traits and the absence of them, the differences. And this pattern forms a twin nested hierarchy (an evolutionary tree) that taxonomy revealed a hundred years before Darwin was alive and just become more robust over time. ......

yes, and all I am saying is that those who deny common ancestry, don't argue that the pattern was a product of chance, therefore any probabilistic arguments are irrelevant. and strawman.

Wrong, because design doesn't predict that these patterns of genetic markers, only common descent does. I challenge you to explain how design predict this, without having to say that the designer just did this way to make it look like everything had evolved from a common ancestor.

For example, a genetic paternity test provides that Individual A is the father of Individual B with a certainty of 99%
How does design provide a competing explanation for this result if these are unrelated?

Of course you can say, but design doesn't mean that a father is unrelated to the child, but when does it stop and how would we know when it stops while the genetic evidence keeps saying, yes these organisms are all related?

Now you are just rambling nonsense. The anthropic principle relates to either of these two things.
1. Humans require a specific environment within the universe to live.
2. Humans require a specific universe (with specific physical properties) to exists.

How the fuck are either of these related to genetics at all??

And we don't just say that we are related with chimps just because we are 97% similar genetically, though that is a strong indication, but it wasn't the definitive factor. It is shared genetic markers that we have: orthologs, ERVs, shared pseudogenes (how does design explain that). Fusion of chromosome number 2, which was predicted by common descent.

How about this answer....
We live in a multiverse, with a potentially infinite number of universes, in most of these universes humans and chimps, don't have all these shared ERVs pseudogenes, proteins.....etc......but in a small minority of these multiverses just by chance, we happen to have all this shared stuff with chimps. We simply happen to live in such universe, if we weren't living in such universe we wouldn't be wondering why we have all this shared stuff and similarities with chimps.

That answer has been shown to be idiotic as I have explained in that quote that the anthropic principle DOES NOT relate to genetics. It only refers to the conditions that require for the existence of humans.
According to the multi verse theory, there are many universes and some have conditions that allow for humans (or just life in general) to exist. And since humans can only exists within a universe with specific conditions, it is not a surprise that we find ourselves in a universe with those conditions. It is a tautology really and that is it.
There is no indication that we should find ourselves within a universe where all life shares genetic markers that indicate common ancestry....if we are somehow not related.

Obviously this is a stupid answer, but my point is that some atheist use the same kind of answer to explain away some theistic arguments, why cant we simply reject those atheists answers for the same reason you would reject my answer?

So just to escape this problem that you can't solve, you resort to arguments that don't apply to the same thing. I can use an argument that argues that cars are better than motorcycles, but the same argument probably doesn't apply to whether hotdogs are better than hamburgers. Similarly the multiverse argument that explains the anthropic principle does not mean it explains shared genetic orthologs, which is a non sequitur. Try an argument that better than "if they play with a toy, why can't I play with it too?"

I will try to help by asking you to answer this question:
According to the genetic markers we share with all life, the certainty that humans are related to other species is 99,99999999999999...etc% I challenge you to explain how design predict the same result, without having to say that the designer just did this way....or the designer just did this way to make it look like everything had evolved from a common ancestor as a test of faith.

 

[Nesslig20]

Some atheistic arguments, or responses, are in fact stupid and silly. I have no compunction agreeing to that. I'm an atheist yet it is entirely obvious to me that some atheists are atheists for bad reasons, or have no, or bad answers to some theistic arguments. In becoming an atheist, one does not magically transform into some sort of flawless logic-computer that only make correct arguments.

This.

In fact, these days, I spend far more effort in correcting these bad arguments than I do arguing with theists.

If I have flaws in my argument, please let me know.

 

[Deleted member 619]

Not spotted anything yet.

 

[leroy]

No they are not, and I explained that in that very quote that I highlighted. It has one benefit creating genetic redundancy. I also mentioned right next to this quote genetic dosage, meaning duplication can have an EFFECT that can be beneficial, thus NOT neutral.

ok with beneficial effect I mean any effect that makes the organism more likely to survive and reproduce.............hopefully you mean the same.


Granted, duplicación might be beneficial, but what you have to do is prove that this specific duplications are beneficial...

Our results entail a simple scenario of opsin evolution. The first opsin originated from the duplication of the common ancestor of the melatonin and opsin genes in a eumetazoan (Placozoa plus Neuralia) ancestor, and an inference of its amino acid sequence suggests that this protein might not have been light-sensitive. Two more gene duplications in the ancestral neuralian lineage resulted in the origin of the R, C, and Go/RGR opsins. Accordingly, the first animal with at least a C, an R, and a Go/RGR opsin was a neuralian progenitor.

if you do that, you will show that at least 1 of the millions of steps required for evolving an eye is possible...

remember this is what I mean with step

Well what i would call a step requires 3 things
1 a genetic change achievable in 1 generation (like a gene duplication for example)
2 it has to be beneficial (something that would be selected by natural selection)
3 it has to represent a step closer towards modern eyes

So do you want me to demonstrate all millions of steps? I thought you wanted to keep this simple?
We don't need to explain ALL the steps that happened. As I said we don't know everything about any subject. We know enough what happened. Eyes evolved and we (the scientists) know the big picture that shows how they evolved and I have the citations to demonstrate this.

No, you don't have to explain how each one of the millions of steps took place, all you have to do is select a statistically significant sample and just explain that sample.....


but the fact that you can not even explain how a single step took place puts your theory in to a very uncomfortable position.

Humans have 49 Cytochrome pseudogenes as a result of many duplication events. What is the chance? The reason why is because so many duplications happen, it is CERTAIN that some will be inherited just by genetic drift alone. The same is with all mutations. There are so many mutations that are largely neutral that it is guaranteed that some of them will spread or even get fixed in the population. That is why we have variations among individuals that don't seem to be of any benefit. If you are or your family members have blond hair and blue eyes or red heads, those traits have no benefits.

Granted, the probability that some neutral mutations become fixed is almost 100%.............however the probability for a specific mutation to become fixed is nearly zero.

If you what to evolve an eye, you need a very specific set of mutations, therefore you do have a probabilistic problem if you what to argue that neutral mutations a genetic drift are responsable for the evolution of the eye.

leroy

So please answer this question, any objection that I might have depends on how you answer this question.
talking about the evolution of sight...........are you a neutralist or a selectionist?

ness

Both. Since there are so many neutral mutation (some that do lead to changes in phenotypes) that get inherited, genetic drift has been proven to be a larger role in the evolution of species. Does that mean natural selection played no role? No, it still does.

nice try, so your strategy is to keep your answer ambiguous, because you know that neutralism has a probabilistic problem that you cant solve, and selectionism has a burden proof that you don't what to carry, namely identify the mutations that could have occurred and prove that they had a benefit.


My question is which of these mechanisms predominated

1 neutral mutation + genetic drift

2 beneficial mutation + selection

I know that you believe that both mechanisms took place, my question is which of these 2 mechanisms predominated in the evolution of eyes.

lets see how long does it take you to answer this question clearly and ambiguously.....or you can simply admit that you don't know .....

ness

According to the multi verse theory, there are many universes and some have conditions that allow for humans (or just life in general) to exist. And since humans can only exists within a universe with specific conditions, it is not a surprise that we find ourselves in a universe with those conditions. It is a tautology really and that is it.
There is no indication that we should find ourselves within a universe where all life shares genetic markers that indicate common ancestry....if we are somehow not related

.


leroy
According to the multi verse theory, there are many universes and some have conditions that allow for humans to observe genetic similarities between chimps and humans. And since this observations can only exists within a universe with specific conditions, that allow humans and chimps to have such similarities it is not a surprise that we find ourselves in a universe with those conditions. It is a tautology really and that is it.

my only point is that using atheist logicone can dismiss the genetic similarity argument very easily. no matter how improbable is it to have similarities just by chance, according to the multiverse hypothesis there are universes where we have all this similarities

hopefully we both agree that this logic is flawed, a very bad response.............well at least Rumraket agrees with me
Remarket

We can, I absolutely agree, reject such an answer as completely idiotic and unsatisfying. One can basically explain away everything with that kind of "answer".

Some atheistic arguments, or responses, are in fact stupid and silly. I have no compunction agreeing to that. I'm an atheist yet it is entirely obvious to me that some atheists are atheists for bad reasons, or have no, or bad answers to some theistic arguments. In becoming an atheist, one does not magically transform into some sort of flawless logic-computer that only make correct arguments.

ness

will try to help by asking you to answer this question:
According to the genetic markers we share with all life, the certainty that humans are related to other species is 99,99999999999999...etc% I challenge you to explain how design predict the same result, without having to say that the designer just did this way....or the designer just did this way to make it look like everything had evolved from a common ancestor as a test of faith.

Granted, Universal Common ancestry is the best explanation for the data, (better than design) my only claim is that there is room for reasonable doubt, for example we do find countless gene trees discordances, that cant be explained and where not predicted by universal common ancestry (echolocation in bats and whales for example)................


as for how could this be explained without common ancestry....

well maybe chimps and humans have these genetic markers in the same place, because they both need them in the same place...........this is obviously an ad hoc, but the thing is that the data is not irreconcilable with design. No one is arguing that these similarities are just happened by chance, it could be that the designer had a bias in creating his creatures with similar genetic markers. (even though I agree, common ancestry explains the data better than design.)

I mean if a designer creates 1000 computer programs independently it wouldn't be surprising to find similarities among these programs, and it wouldn't be surprising to fin that some of these programs are more similar to each other than to the rest of the programs.


so just to be clear...

yes common ancestry is the best explanation for sheered genetic markers, but I don't see why this data should be devastating for intelligent design, and any honest person should admit that there are incorrect predictions in the universal common ancestry, which leave the door open for reasonable doubt

 

[he_who_is_nobody]

Granted, Universal Common ancestry is the best explanation for the data, (better than design) my only claim is that there is room for reasonable doubt, for example we do find countless gene trees discordances, that cant be explained and where not predicted by universal common ancestry (echolocation in bats and whales for example)................

[emphasis added]

:docpalm:

On July 19th, 2014 Inferno[/url]"]In the exact way Dr. Whittington explained that the amino acids converged in platypus and snakes, meaning the protein sequence, so also do the protein sequences in bats and toothed whales. This is what you get wrong and that's why your example is not valid. Let me make this absolutely clear: When comparing the gene or nucleotide sequence, bats and toothed whales are correctly classified. If the protein sequence is compared, bats are classified with toothed whales. That's the whole deal. The gene sequences are not the same. This is made absolutely clear in a paragraph I quoted earlier:

Convergent sequence evolution between echolocating bats and dolphins (2010)[/url]"]To test whether convergent changes in bat Prestin genes have also occurred in echolocating whales, we sequenced the entire gene in a range of echolocating toothed whales and non-echolocating baleen whales, as well as additional bats (see Table S1 in the Supplemental Data available on-line with this issue). Trees based on nucleotide alignments from this larger dataset strongly supported the accepted species tree topology, albeit with the clustering of echolocating bats reported earlier [3]. However, in trees based on amino acid sequences, constructed using a range of different phylogenetic methods, we found that the echolocating dolphins now formed a well-supported group with echolocating horseshoe and Old World leaf-nosed bats (node posterior probability = 0.99 or 0.94 depending on the analysis), members of which emit Doppler-sensitive signals dominated by a constant frequency (CF) component [6] ( Figure 1A). Intriguingly, the addition of the sperm whale, which appears to echolocate at much lower frequencies [7], was seen to decrease support for this convergent signal, leading to the cetaceans and bats both forming monophyletic groups. The extent of sequence convergence between bats and whales was thus not sufficient to unite these clades when non-dolphin odontocetes were included in the analysis.

Do you understand your mistake, can we move on?

It's even more fun that you accuse me of not reading the article when you make a grave mistake:

However, in trees based on amino acid sequences, constructed using a range of different phylogenetic methods, we found that the echolocating dolphins now formed a well-supported group with echolocating horseshoe and Old World leaf-nosed bats.

You quote the passage that disproves what you claim, yet you fail to register that. Reading comprehension fail if ever there was one.

Now as I said, you can have the same amino acid sequence even if the underlying genetic code is different (I even showed that using the BLASTed sequences) and you can have very similar amino acids forming basically identical proteins, which is what they found. Don't let the pop-science articles cloud your judgement on this.

 

[Nesslig20]

No they are not, and I explained that in that very quote that I highlighted. It has one benefit creating genetic redundancy. I also mentioned right next to this quote genetic dosage, meaning duplication can have an EFFECT that can be beneficial, thus NOT neutral.

ok with beneficial effect I mean any effect that makes the organism more likely to survive and reproduce.............hopefully you mean the same.

Repeat:

Loss of Genetic Redundancy in Reductive Genome Evolution[/url]"]Biological systems evolved to be functionally robust in uncertain environments, but also highly adaptable. Such robustness is partly achieved by genetic redundancy, where the failure of a specific component through mutation or environmental challenge can be compensated by duplicate components capable of performing, to a limited extent, the same function. Highly variable environments require very robust systems. Conversely, predictable environments should not place a high selective value on robustness. Here we test this hypothesis by investigating the evolutionary dynamics of genetic redundancy in extremely reduced genomes, found mostly in intracellular parasites and endosymbionts. By combining data analysis with simulations of genome evolution we show that in the extensive gene loss suffered by reduced genomes there is a selective drive to keep the diversity of protein families while sacrificing paralogy. We show that this is not a by-product of the known drivers of genome reduction and that there is very limited convergence to a common core of families, indicating that the repertoire of protein families in reduced genomes is the result of historical contingency and niche-specific adaptations. We propose that our observations reflect a loss of genetic redundancy due to a decreased selection for robustness in a predictable environment.

Evolution of genetic redundancy[/url]"]Genetic redundancy means that two or more genes are performing the same function and that inactivation of one of these genes has little or no effect on the biological phenotype. Redundancy seems to be widespread in genomes of higher organisms1, 2, 3, 4, 5, 6, 7, 8, 9. Examples of apparently redundant genes come from numerous studies of developmental biology10, 11, 12, 13, 14, 15, immunology16,17, neurobiology18,19 and the cell cycle20,21. Yet there is a problem: genes encoding functional proteins must be under selection pressure. If a gene was truly redundant then it would not be protected against the accumulation of deleterious mutations. A widespread view is therefore that such redundancy cannot be evolutionarily stable. Here we develop a simple genetic model to analyse selection pressures acting on redundant genes. We present four cases that can explain why genetic redundancy is common. In three cases, redundancy is even evolutionarily stable. Our theory provides a framework for exploring the evolution of genetic organization.

Granted, duplicación might be beneficial, but what you have to do is prove that this specific duplications are beneficial...

Our results entail a simple scenario of opsin evolution. The first opsin originated from the duplication of the common ancestor of the melatonin and opsin genes in a eumetazoan (Placozoa plus Neuralia) ancestor, and an inference of its amino acid sequence suggests that this protein might not have been light-sensitive. Two more gene duplications in the ancestral neuralian lineage resulted in the origin of the R, C, and Go/RGR opsins. Accordingly, the first animal with at least a C, an R, and a Go/RGR opsin was a neuralian progenitor.

As I said, it doesn't have to be beneficial and:

Selection in the evolution of gene duplications[/url]"]
The results of this analysis indicate that recently duplicated paralogs evolve faster than orthologs with the same level of divergence and similar functions, but apparently do not experience a phase of neutral evolution. We hypothesize that gene duplications that persist in an evolving lineage are beneficial from the time of their origin, due primarily to a protein dosage effect in response to variable environmental conditions; duplications are likely to give rise to new functions at a later phase of their evolution once a higher level of divergence is reached.

if you do that, you will show that at least 1 of the millions of steps required for evolving an eye is possible...

remember this is what I mean with step

Well what i would call a step requires 3 things
1 a genetic change achievable in 1 generation (like a gene duplication for example)
2 it has to be beneficial (something that would be selected by natural selection)
3 it has to represent a step closer towards modern eyes

Yes, I remember that stupid requirement...Remember why?

Why would it have to be achievable in 1 generation? Why not 2, or 5, or a hundred? The answer is that it doesn't.
Why would it have to be "positive" rather than neutral? It doesn't. It could even be slightly deleterious and still fix by drift in a small population, or substantially deleterious yet hitchike with another beneficial allele.
Why would someone have to provide a step by step path at this level of detail? Do you even have any other beliefs which are supported by such a level corroboration? Of course you don't.
Isn't it obvious you're deliberately setting the bar irrationally high? Yes, yes it is.
......................
No. I'm obviously not claiming all of eye-evolution was achieved by genetic drift, that would be preposterous. Rather, I'm merely saying that not all of the "steps" have to be beneficial. We know for a fact that there are complex phenotypes who's evolutionary history include necessary neutral mutations that fixed by genetic drift.
For example, the evolution of chloroquine resistance in plasmodium falciparum requires multiple neutral mutations along the way.
And in the Long-Term Evolution Experiment, the cit+ phenotype requires at least one neutral, potentiating mutation.

each change (or at least most of them) would have to be beneficial

This is simply not true, and the fact that it isn't true has been pointed out six ways from Sunday.
You're operating from an entirely false premise. Not only are they not required to be beneficial, they're not even required to be beneficial in the context of their environment. There's no sense in which your contention isn't fundamentally wrong.

And you admitted that requirement #2 isn't necessary.

granted, not all of the steps have to be beneficial.

So why include that requirement again? Suffer from short term memory? From looking at old discussions between you and others and from my own experience by arguing with you, I think you do.
You frequently bring up points back even though they have been refuted before, like that Bat/Dolphin echolocation thing that you brought back some time later after I have shown that to be flawed. Stop using PRATTS.

So do you want me to demonstrate all millions of steps? I thought you wanted to keep this simple?
We don't need to explain ALL the steps that happened. As I said we don't know everything about any subject. We know enough what happened. Eyes evolved and we (the scientists) know the big picture that shows how they evolved and I have the citations to demonstrate this.

No, you don't have to explain how each one of the millions of steps took place, all you have to do is select a statistically significant sample and just explain that sample.....

Which I did. Read all those citations.

but the fact that you can not even explain how a single step took place puts your theory in to a very uncomfortable position.

pffff, I have gone from A to B to C all the way to Z but you keep demanding more and more such that you can pretend that I have not done anything.

Humans have 49 Cytochrome pseudogenes as a result of many duplication events. What is the chance? The reason why is because so many duplications happen, it is CERTAIN that some will be inherited just by genetic drift alone. The same is with all mutations. There are so many mutations that are largely neutral that it is guaranteed that some of them will spread or even get fixed in the population. That is why we have variations among individuals that don't seem to be of any benefit. If you are or your family members have blond hair and blue eyes or red heads, those traits have no benefits.

Granted, the probability that some neutral mutations become fixed is almost 100%.............however the probability for a specific mutation to become fixed is nearly zero.

Just like the probability of both of us being born form the gamete cells of our parents are astronomical. Seriously look up independent assortment and recombinations. That makes any particular genetic combination that result in YOU or ME practically impossible:

Yet here we are!

If you what to evolve an eye, you need a very specific set of mutations, therefore you do have a probabilistic problem if you what to argue that neutral mutations a genetic drift are responsable for the evolution of the eye.

Wrong, there are more ways to solve a particular problem. Animals (even some non animal organisms) have managed to evolve eyes multiple times independently (although most animals inherited a basic tool kit like opsins, i.e. light sensitive proteins form a common ancestor but have enhanced their eyes independently...) with different mutations, resulting in different "designs" but having the same function.

So please answer this question, any objection that I might have depends on how you answer this question.
talking about the evolution of sight...........are you a neutralist or a selectionist?

Both. Since there are so many neutral mutation (some that do lead to changes in phenotypes) that get inherited, genetic drift has been proven to be a larger role in the evolution of species. Does that mean natural selection played no role? No, it still does.

nice try, so your strategy is to keep your answer ambiguous, because you know that neutralism has a probabilistic problem that you cant solve, and selectionism has a burden proof that you don't what to carry, namely identify the mutations that could have occurred and prove that they had a benefit.

1. No I said BOTH, that is not ambiguous. Natural selection and genetic drift are NOT mutually exclusive mechanisms in the sense of no 100% this or 100% that. They can both contribute to the fixation or elimination of mutations in a population with varying degrees depending on the population size. Stop thinking in black or white.
2. Neutralism doesn't have a probabilistic problem as I have already explained. There are extremely unlikely events like us being born if you calculated it as if with foresight, but that is the problem. We note this things in hindsight, thus it doesn't matter how likely the event that happened could happen. Once it happened, the odds of it happening are 100%.

"That a particular specified event or coincidence will occur is very unlikely. That some astonishing unspecified events will occur is certain. That is why remarkable coincidences are noted in hindsight, not predicted with foresight."
—David G. Myers

My question is which of these mechanisms predominated
1 neutral mutation + genetic drift
2 beneficial mutation + selection
I know that you believe that both mechanisms took place, my question is which of these 2 mechanisms predominated in the evolution of eyes.
lets see how long does it take you to answer this question clearly and ambiguously.....or you can simply admit that you don't know .....
[/quote]

You don't have to wait long, since I already have answered that question, though not clearly. I said this

Both. Since there are so many neutral mutation (some that do lead to changes in phenotypes) that get inherited, genetic drift has been proven to be a larger role in the evolution of species. Does that mean natural selection played no role? No, it still does.

So drift dominates mostly during evolution of species, especially when the population size is small, which it often is. So you might think that the way life evolved in this particular way is very unlikely, you would be right. If you rewind the tape to about 1 billion years ago and let everything play out on its own, chances are that familiar species won't ever evolve. You would still have bacteria and maybe even eukaryotes if they already existed 1 billion years ago, however there would be other things that would be unrecognizable. Maybe similar in the same way a dolphin is similar to a shark or a bat is to a bird, but you won't find anything that you could say that is a mammal or a bird. Just like if you rewind the tape back before you were a zygote, when you mom and dad had that very special night, changes are that a different sperm cell fertilized the egg, so instead of you being born, a different human being equivalent to your brother or sister would have been born which was FAAARRR more likely.

But again, there is a different in noticing improbable events in foresight and hindsight.

According to the multi verse theory, there are many universes and some have conditions that allow for humans (or just life in general) to exist. And since humans can only exists within a universe with specific conditions, it is not a surprise that we find ourselves in a universe with those conditions. It is a tautology really and that is it.
There is no indication that we should find ourselves within a universe where all life shares genetic markers that indicate common ancestry....if we are somehow not related

.
According to the multi verse theory, there are many universes and some have conditions that allow for humans to observe genetic similarities between chimps and humans. And since this observations can only exists within a universe with specific conditions, that allow humans and chimps to have such similarities it is not a surprise that we find ourselves in a universe with those conditions. It is a tautology really and that is it.

Using an argument and replacing certain words to make a parody only works when you use it in the correct context that is applicable. Otherwise it will make you look like an idiot.

"According to the multi verse theory, there are many universes and some have conditions that allow for humans to pick there noses. And since this observation can only exists within a universe with specific conditions that allows humans pick their nose, it is not a surprise that we find ourselves in a universe with those conditions. It is a tautology really and that is it."

What you keep missing is that the argument applies to conditions that allows humans to LIVE.
There is no indication that we must live in a universe with specific conditions that allows us to pick our noses thus there is no reason that should find ourselves in such a universe, and there is no indication that we should find ourselves within a universe where all life shares genetic markers that indicate common ancestry....if we are somehow not related. This last part you omitted from your parody, because that demonstrates why the parody is so dumb.

So answer this: According to the multiverse, we can only live in a universe that allows us to live in, which is why we are living in such a universe, which (barely) allows us to live.
Why should we find ourselves in a universe that includes phylogenetic markers indicating common ancestry all life on earth, IF we don't share a common ancestry??

my only point is that using atheist logicone can dismiss the genetic similarity argument very easily. no matter how improbable is it to have similarities just by chance, according to the multiverse hypothesis there are universes where we have all this similarities

However, there is no reason why we should be living in such a universe. That is the point of logic you are missing.

hopefully we both agree that this logic is flawed, a very bad response.............well at least Rumraket agrees with me
Remarket

We can, I absolutely agree, reject such an answer as completely idiotic and unsatisfying. One can basically explain away everything with that kind of "answer".

Some atheistic arguments, or responses, are in fact stupid and silly. I have no compunction agreeing to that. I'm an atheist yet it is entirely obvious to me that some atheists are atheists for bad reasons, or have no, or bad answers to some theistic arguments. In becoming an atheist, one does not magically transform into some sort of flawless logic-computer that only make correct arguments.

I fully agree with that statement. However the point is that this parody isn't an accurate representation of the original argument of the multiverse which only states about why we live in a universe that allows us to live, not why we live in a universe that allows us to pick our noses or to observe shared genetic orthologs among different taxa. And Rumraket never states that your parody is an accurate representation or usage of the multiverse argument that shows how flawed the "atheist logic" (emphasis on the quotes) is in that particular instance. Otherwise I would disagree with him. Your parody about the multiverse just shows how illogical your logic skills are.

will try to help by asking you to answer this question:
According to the genetic markers we share with all life, the certainty that humans are related to other species is 99,99999999999999...etc% I challenge you to explain how design predict the same result, without having to say that the designer just did this way....or the designer just did this way to make it look like everything had evolved from a common ancestor as a test of faith.

Granted, Universal Common ancestry is the best explanation for the data, (better than design) my only claim is that there is room for reasonable doubt, for example we do find countless gene trees discordances, that cant be explained and where not predicted by universal common ancestry (echolocation in bats and whales for example)................

:facepalm: I will just have to copy paste my first response to this bat/dolphin PRATT, again!!

The problem is that true chimeras have been found.

For example Echolocation is bats and dolphins.

Bats and dolphins both devolved a complex system of echolocation. You can´t explain this with common ancestry because bats and dolphins are not close relatives and their common ancestors was a mammal without a system of echolocation.
This means that dolphins and bats developed this ability independently.

Yes, it's called convergent evolution. Where two different lineages independently evolve features that have the same function.
I guess, I should have informed you about it earlier. I don't know why you didn't use this as an example of convergence.

All three animals (one extinct of course) use essentially the same bones in the structure of their wings: Humerus, ulna, radius, etc.
And I expect, because they use the same bones, similar genes would be involved in building their wings. However, there are notable differences.
Birds use three finger bones (now fused together) and their wings use feathers.
Bats use four finger bones as the frame of the wing which uses a membrane, with the "thumb" sticking out the wing.
Pterosaurs used a ridiculously elongated pinky finger to support their wing membrane, but the membrane, though similar looking, was very unlike the membranes of bats. The really advanced pterosaur had membranes full of various fibers including muscle, such that they had an incredible flight control. Some even had resperatory air sacs extending from cavities inside their bones into the wing membranes.
Even though they use the same bones, which they inherited from their common ancestor, for their wings, they modified those bones into wings by different means, which doesn't matter, as long as it works.
In order to fly, it requires several things like being light weight and have wings: thin airfoil-, streamlined structures with a large surface area that can produce the necessary lift. Which is what all these three examples did develop, but again by different means.
Similar (analogous) things can evolve independently, but not identical things
Thus this doesn't violate phylogeny. As with the echolocation of bats and dolphins, which I will explain next.

Ecolocation in bats and dolphins is almost identical even at a molecular level (same proteins same genes)
Finding two unrelated animals with echolocation is as bad as finding a horse with feathers.

Not quite as bad, which I will explain in a moment. But first addressing your claims:
1 "Ecolocation in bats and dolphins is almost identical"
2 "even at a molecular level (same proteins same genes)"

#1 Let's look at how the echolocation of bats and dolphins work.
In order to echo locate you need two basic things. One, the ability to generate and emit sound waves and two receive the echo it produces. Again, how you manage to do this, doesn't matter.
Bats generate ultrasound with their larynx and emit it through their open mouth or in some cases their nostrils.

Dolphins on the other hand produce their sound by passing air from the bony nares through the phonic lips. The sound is reflected by the animals thick concave bone of the cranium and the sound is modulated by the fatty organ called the 'melon' almost like an acoustic lens, focussing the sound waves in one direction.

Very different mechanisms for generating and emitting sound. Although receiving the echo is the same. They use their ears, which they did inherited from a common ancestor.
Starting to see a pattern here?

Note that the only thing you need to echolocate is emitting sound and receiving echo. You might ask, we can do both so why can't we echolocate. Well surprisingly we can, people who are blind often learn to echo locate and in some extreme cases blind from birth just develop the skill naturally, but we suck at it compared to those that can emit much more sound and have very sensitive hearing.


The key is sensitive hearing and all mammals have this trait because they have an inner ear structure with unique auditory ossicles that can pick up sounds almost no other group of tetrapods can, which evolved in the ancestors of mammals.

Once again, common ancestry, which is why almost all echolocating animals are mammals and the ones that are really good at it are all mammals. But it is still amazing that humans can echolocate like the superhero daredevil (the real batman). People like the one in the video actually report a description of their echo sense as visual patterns. And brain activity of these people support that they process auditory information to produce a visual image, a form of synesthesia that makes sound translated into sight and we all have the potential to do that.

Too bad our feet aren't sensitive enough for echolocation, because that would've been awesome.

#2: Almost identical at the molecular level (same proteins same genes).
I looked that the citation you provided, but nowhere does it say that the genes where identical, nor in the original article.

The only similar statement that it said was:
"in 2010, Stephen Rossiter, an evolutionary biologist at Queen Mary, University of London, and his colleagues determined that both types of echolocating bats, as well as dolphins, had the same mutations in a particular protein called prestin, which affects the sensitivity of hearing. Looking at other genes known to be involved in hearing, they and other researchers found several others whose proteins were similarly changed in these mammals."

Notice that it doesn't say that the proteins and genes are identical. The mutations where identical and they happen in the same genes. Prestin in particular which is involved in hearing, not surprising since both bats and dolphins use hearing in echolocation.

But the genes as a whole are not identical. Let me demonstrate.
I took the nucleotide sequences of the prestin genes of both echolocating bats and echolocating dolphins and compare it with the sequences of their relatives that don't echolocate. You can do this too using NCBI blast.

Let's do this science style.

Question: What are the relationships between the gene sequences of the gene prestin of echolocating animals (certain bats and dolphins) and their close relatives.

Hypothesis 1 (common ancestry): Even though prestin of dolphins and certain bats contain similar changes as an adaptation towards echolocation, the relationship between them and their relatives should still follow the model of common ancestry. The prestin of echolocating bats should be more similar to that of non-echolocating bats and that of dolphins should be more similar relatives like other Cetaceans that don't echolocate.

Hypothesis 2 (Identical at the molecular level, same proteins same genes): Since prestin is identical in both echolocating bats and dolphins, they should be more similar to each other, even more then sequences of those that are supposedly more closely related to them than either one are to each other.

Data:
Prestin cDNA sequences of:
1. Echolocating animals
- Bottlenose Dolphin
- Little brown bat

2. Non echolocating animals
Close relative of dolphins:
- Mink whale
Close relative of echolocating bats:
- Large Flying Fox

Methods: NCBI blast

Results:
1 Close relative comparisons (echo locators on their non echo locator relative).
- Bottlenose Dolphin / Mink whale = 97% match
- Little brown bat / Large flying fox = 93% match

2. Echolocators comparisons
- Little brown bat / Bottle Nose dolphin = 92% match

Conclusion:
There is a closer match between the echo locators and their close relatives then there is between the echo locators themselves, which was expected by the hypothesis based on common ancestry.

So you challenge is:
¿how do you explain echolocation in bats and dolphins? And whatever explanation that you provide, ¿what can´t that explanation could be used to explain feathers in horses?
¿what is fundamentally different between horses with feathers and bats with “dolphin-like echolocation”?

The difference is that horses with feathers have actual feathers, identical to those of the feathers of birds.
Bats don't have dolphin echo location, which is why you said "dolphin-like" instead.

And note that echo location requires only the ability to make sound waves and sensitive hearing to detect the echo, which even humans who usually don't echolocate still have and with training can even develop a weak form of echolocation. Feathers on the other hand require allot more then that. Feathers you see on flying birds are a highly complex structure that evolved through several sequential stages of development over a span of over a hundred and fifty million years.

Now, different types of animals have independently evolved different types of eyes which are unique to that lineage (again, concordant with common ancestry), like vertebrates have their unique type of eye with the blind spot and all Cephalopods have their unique eye structure.

You will never find a Vertebrate with a Cephalopod eye or vise versa. Isn't that odd?

And you also can have similar mutations occurring within similar genes that have similar effects independently in different lineages, however (in the case of feathers) such a precise alignment of this sequence with these particular developments over such a long period of time, could not have evolved twice. Fully developed flight feathers are a one time occurrence. They have first appeared in theropod dinosaurs and were inherited by birds and are exclusive to this group.

Why ask that again, when I have answered that several times!!?? Also disagreement between the species trees and the trees of the individual genes of those species is to be expected if you have learned anything about population genetics or specifically incomplete lineage sorting. It is the understanding that a particular mutation only happens in one individual and it needs time to spread throughout. When a population split into two (or more) species, it is the case that this mutation isn't fixed yet and thus the descended population could either lose or fixate the mutation. Also gene flow between species shortly after the split can be a factor as well.

Nature article "Comparative primate genomics: emerging patterns of genome content and dynamics"[/url]"]

a | Incomplete lineage sorting can produce discrepancy between the phylogenetic tree for a specific gene or a genomic segment and the overall species-level phylogenetic tree. If an ancestral species is polymorphic (in this case, it is segregating Alleles A and B) and divides into two descendent lineages, then both alleles can be retained in the two daughter lineages. If one of these lineages divides again relatively soon, then all three species lineages may carry both alleles. Over time, each lineage will lose one or the other allele owing to genetic drift or selection. In this case, Species 1 retains Allele A and Species 3 retains Allele B. For this genomic segment, Species 2 will seem to be more closely related to either Species 1 or Species 3 depending on whether it retains Allele A or Allele B. Retention of Allele B would mean that this genomic segment matches the overall species-level phylogenetic tree, but retention of Allele A would lead to discrepancy. Analyses of whole-genome sequences for humans, chimpanzees and gorillas indicate that gene trees for a substantial portion of the genome do not match the overall species-level phylogeny, which places chimpanzees as closer relatives to humans than to gorillas19. b | Gene flow between diverging lineages is shown. Evidence from various primate species, especially for the ancestors of extant apes and humans, indicates that the process that produced the extant evolutionary lineages did not consist of rapid separation and immediate complete genetic isolation. Rather, recent analyses52 suggest that in several cases, new evolutionary lineages can diverge and accumulate genetic differences despite maintaining some degree of genetic exchange (that is, gene flow). The situation depicted here shows three lineages arising from a common ancestor. In both cases of species-level divergence, there is gene flow (horizontal bars) between lineages. Allele B is transferred from one lineage to another through this process but is lost from the recipient lineage owing to either genetic drift or selection. Allele C is transferred between lineages and increases in frequency such that it is retained for an extended period, and it may therefore influence the evolutionary trajectory of the recipient lineage (Species 2). Rather than occurring as one discrete episode, the gene flow between diverging lineages probably decreases over time and eventually fades out.

I believe someone else already explained this to you. What a shock. :roll:

If compere just the human, chimp and gorilla, DNA which are the animals that have been studied in more detail, 30% of the genes form discordant trees. We are not talking about insignificant exceptions, we are talking about 30% of the genome.
http://www.evolutionnews.org/2012/03/gorilla_genome_057391.html
If animals could have been organized in a nearly perfect nested hierachy then I would accept evolution, it would be lunatic to argue that God created things as if evolution where true.

Wrong. This has already been discredited as another creationist misrepresntation of the actual data:
From my favorite theistic evolution blog: https://letterstocreationists.wordpress.com/2012/03/17/gorilla-orangutan-chimp-and-human-genomes-population-genetics-and-intelligent-design/
And good ol PZ myers: http://freethoughtblogs.com/pharyngula/2012/03/11/a-tiny-bit-of-knowledge-is-a-dangerous-thing/

To sum it up though:

So the creationist argument against evolution on the basis of incomplete lineage sorting is very, very silly. The only way you would fail to see ILS is if every genetic difference between two species emerged simultaneously, in lockstep, in one grand swoop. That is, the observation of ILS contradicts creationism, not evolution.

These observations CAN be explained and WERE predicted based on common ancestry.

well maybe chimps and humans have these genetic markers in the same place, because they both need them in the same place

That is not true at all, many genetic markers don't affect the function of that DNA. Single nucleotide polymorphism often are just random genetic variations within a population and they don't need to be in the same place. ERVs is a good example. Some ERV genes have been coopted for a function, but most are dormant viral genes that don't do anything. Gene get expressed wherever they are on the DNA. That is why we can randomly insert a gene in a genome and if it is inserted intact, it will be expressed no matter where it lands on.

...........this is obviously an ad hoc, but the thing is that the data is not irreconcilable with design.

The only way it is reconcilable is if the designer just made life look like as if it had evolved from a common ancestor, which is not a reconciliation, just an ad hoc excuse.

No one is arguing that these similarities are just happened by chance, it could be that the designer had a bias in creating his creatures with similar genetic markers. (even though I agree, common ancestry explains the data better than design.)

.........I have no words.

I mean if a designer creates 1000 computer programs independently it wouldn't be surprising to find similarities among these programs, and it wouldn't be surprising to fin that some of these programs are more similar to each other than to the rest of the programs.

However you wouldn't see anything like this:

Or this

so just to be clear...
yes common ancestry is the best explanation for shared genetic markers, but I don't see why this data should be devastating for intelligent design,

The fact that we have overwhelming evidence for common descent should already leave any alternative obsolete, but it isn't such that design would be a reasonable alternative if evolution were wrong. Intelligent design has failed every test to qualify as a working hypothesis, much less a scientific theory.

and any honest person should admit that there are incorrect predictions in the universal common ancestry, which leave the door open for reasonable doubt

If there were, an honest person would, as of today, no one has shown such predictions.

 

[leroy]

I will just have to copy paste my first response to this bat/dolphin PRATT, again!!


.

Alll your comments about wings, convergent evolution, etc. are very interesting but irrelevant, there are 3 facts that any honest person has to grant, and that you haven't done anything to disprove them.


1Accepting Common Ancestry and our current phylogenetic tree, implies that bats and dolphins suffered from the same mutations in the same loci 200 independent times
http://www.nature.com/nature/journal/v502/n7470/full/nature12511.html

2 There is no current explanation on how could 2 independent clades could have sufferer form the same mutations 200 independent times, even assuming strong selective pressure, it is very unlikely for 2 organisms to have the same random mutation in the same place. (let alone 200)

3 evolution (common ancestry) predicted that similarities in echolocation would have been superficial (like wings in bats and birds) similarities where not expected at a genetic level.

none of this disproves common ancestry, it simply proves that there are some missing pieces in the puzzle.

Rumraket wrote:
Some atheistic arguments, or responses, are in fact stupid and silly. I have no compunction agreeing to that. I'm an atheist yet it is entirely obvious to me that some atheists are atheists for bad reasons, or have no, or bad answers to some theistic arguments. In becoming an atheist, one does not magically transform into some sort of flawless logic-computer that only make correct arguments.


This.

hackenslash

In fact, these days, I spend far more effort in correcting these bad arguments than I do arguing with theists

well hackenslash you have an opportunity to correct Ness, please explain to him that those 3 points are correct and uncontroversially true.

ness

Just like the probability of both of us being born form the gamete cells of our parents are astronomical. Seriously look up independent assortment and recombinations. That makes any particular genetic combination that result in YOU or ME practically impossible:

well, then why are you making such a big deal with orthologs mutations in chimps and humans and probabilities, ? by you logic my existence is more improbable than similarities between chimps and humans

1 So ether drop that kind of reasoning and admit that it is fallacious

2 or drop common ancestry and your improbability arguments.

please choose 1 or 2.



p

ffff, I have gone from A to B to C all the way to Z but you keep demanding more and more such that you can pretend that I have not done anything.

:lol: :lol: :lol: :lol: :lol: :lol: :lol:

no you have not. you have to provide a statistical significan sample (or atleast a single example) of the steps needed to evolve an eye, you haven't done that.

I already told you what I mean by step.

Well what i would call a step requires 3 things
1 a genetic change achievable in 1 generation (like a gene duplication for example)
2 it has to be beneficial (something that would be selected by natural selection)
3 it has to represent a step closer towards modern eyes

leroy

My question is which of these mechanisms predominated
1 neutral mutation + genetic drift
2 beneficial mutation + selection

second time I ask the question and second time that you did not answer,

ness (your supposed answer)

So drift dominates mostly during evolution of species, especially when the population size is small, which it often is. So you might think that the way life evolved in this particular way is very unlikely, you would be right. If you rewind the tape to about 1 billion years ago and let everything play out on its own, chances are that familiar species won't ever evolve. You would still have bacteria and maybe even eukaryotes if they already existed 1 billion years ago, however there would be other things that would be unrecognizable. Maybe similar in the same way a dolphin is similar to a shark or a bat is to a bird, but you won't find anything that you could say that is a mammal or a bird. Just like if you rewind the tape back before you were a zygote, when you mom and dad had that very special night, changes are that a different sperm cell fertilized the egg, so instead of you being born, a different human being equivalent to your brother or sister would have been born which was FAAARRR more likely.

We are not talking about mutations in general, we are talking about the specific mutations responsable of evolving the eye (human eye for example) where this mutations mainly neutral or beneficial? ....which mutations predominated in the evolution of the human eye?............(or feel free to use some other eye)

ness

Using an argument and replacing certain words to make a parody only works when you use it in the correct context that is applicable. Otherwise it will make you look like an idiot.

"According to the multi verse theory, there are many universes and some have conditions that allow for humans to pick there noses. And since this observation can only exists within a universe with specific conditions that allows humans pick their nose, it is not a surprise that we find ourselves in a universe with those conditions. It is a tautology really and that is it."

What you keep missing is that the argument applies to conditions that allows humans to LIVE.
There is no indication that we must live in a universe with specific conditions that allows us to pick our noses thus there is no reason that should find ourselves in such a universe, and there is no indication that we should find ourselves within a universe where all life shares genetic markers that indicate common ancestry....if we are somehow not related. This last part you omitted from your parody, because that demonstrates why the parody is so dumb.

in fact the parody and the analogy is valid.


according to the multiverse hypothesis, there are universes where chimps and humans have orthologues mutations, simply by chance.

given that we live in a universe where we observe those similarities, it obvious that we live in such universe.


observers that can observe themselves in a universe where chimps and humans have orthologues mutations can only exist in universes where they have such orthologs mutations.

this is analogous to.....

observers that observe themselves living in a universe can only exist in a universe where they can exist and make such observations.

 

[Nesslig20]

Just to be clear, I have expanded my previous response before I saw this post:

I will just have to copy paste my first response to this bat/dolphin PRATT, again!!
.

Alll your comments about wings, convergent evolution, etc. are very interesting but irrelevant, there are 3 facts that any honest person has to grant, and that you haven't done anything to disprove them.

I have written quite more than that, bear in mind. I have demonstrated that the echolocating mechanism in bats and dolphins are quite different, but the similarities are due to common descent like they use their mammalian hearing to receiver the echo. I also showed that the gene prestin is more similar between close relatives of the echo locators rather than between the echo locators themselves, which contradicted your statement that the genes were identical and that the trees build from these genes would show that echolocating bats and dolphins are more closely related than their non echolocating relatives.

Question: What are the relationships between the gene sequences of the gene prestin of echolocating animals (certain bats and dolphins) and their close relatives.

Hypothesis 1 (common ancestry): Even though prestin of dolphins and certain bats contain similar changes as an adaptation towards echolocation, the relationship between them and their relatives should still follow the model of common ancestry. The prestin of echolocating bats should be more similar to that of non-echolocating bats and that of dolphins should be more similar relatives like other Cetaceans that don't echolocate.

Hypothesis 2 (Identical at the molecular level, same proteins same genes): Since prestin is identical in both echolocating bats and dolphins, they should be more similar to each other, even more then sequences of those that are supposedly more closely related to them than either one are to each other.

Data:
Prestin cDNA sequences of:
1. Echolocating animals
- Bottlenose Dolphin
- Little brown bat

2. Non echolocating animals
Close relative of dolphins:
- Mink whale
Close relative of echolocating bats:
- Large Flying Fox

Methods: NCBI blast

Results:
1 Close relative comparisons (echo locators on their non echo locator relative).
- Bottlenose Dolphin / Mink whale = 97% match
- Little brown bat / Large flying fox = 93% match

2. Echolocators comparisons
- Little brown bat / Bottle Nose dolphin = 92% match

Conclusion:
There is a closer match between the echo locators and their close relatives then there is between the echo locators themselves, which was expected by the hypothesis based on common ancestry.

You only mentioning my wings example as to show what convergence as if this is the only thing I said, while omitting this important part with the gene comparison, just shows how dishonest you are. Any honest person would at least admit his errors and never use old refuted point again and again, but you are not honest.

And convergent evolution ain't irrelevant since your dolphin/bat example is exactly that, whether you want to accept it or not. Even you own citations mention convergent evolution. It is in the DAMN title!! Don't pretend this is irrelevant.

1Accepting Common Ancestry and our current phylogenetic tree, implies that bats and dolphins suffered from the same mutations in the same loci 200 independent times
http://www.nature.com/nature/journal/v502/n7470/full/nature12511.html

There is no such thing as "suffering" from a mutation, unless the mutation is harmful, which of course these weren't. The article noted that of the 805,053 amino acids within 2,326 orthologous coding gene sequences only 200 were found to be convergent. That is not very big considering the vast data they had to sift through. Also the mutations didn't have to be identical since different mutations can result in the same amino-acid sequences, which is what they looked at. They didn't look at genetic sequences, they looked at amino-acid sequences.

For example, a missense mutations that changes the codon
AAU to ACU
would change the amino acid from Asn to Thr.

And if you change the codon
GCU to ACU
it would change the amino acid from Ala to Thr.

Different codons changed by different mutations into still different codons, but resulting in the same amino acid being translated.

I and others have already explained this too.

2 There is no current explanation on how could 2 independent clades could have sufferer form the same mutations 200 independent times, even assuming strong selective pressure, it is very unlikely for 2 organisms to have the same random mutation in the same place. (let alone 200)

Very unlikely as in 200 out of 805,053 (0,024%) of the time, which don't need to be identical mutations.

3 evolution (common ancestry) predicted that similarities in echolocation would have been superficial (like wings in bats and birds) similarities where not expected at a genetic level.

Correction, similarities were not expected at the protein/amino acid level, since they looked at the amino acid sequence, not the genetic sequence. And even if it was a surprise, now we see that amino acids substitutions can happen independently 200 out of 805053 times between lineages that diverged hundreds of thousands of generations ago.

Surprises doesn't mean, the whole theory is wrong or the theory is incorrect in part. A new exciting discovery was made that no one expected, but the results didn't contradicted anything. Among other surprises the article showed is that many of the genes linked to vision showed convergence as well, meaning that vision could be linked to echolocation, but that surprise doesn't show that anybody was wrong about vision or echolocation.

none of this disproves common ancestry, it simply proves that there are some missing pieces in the puzzle.

If the puzzle was your brain and the missing pieces was the cognitive ability to listen to the same answers that were given a thousand times before.

Rumraket wrote:
Some atheistic arguments, or responses, are in fact stupid and silly. I have no compunction agreeing to that. I'm an atheist yet it is entirely obvious to me that some atheists are atheists for bad reasons, or have no, or bad answers to some theistic arguments. In becoming an atheist, one does not magically transform into some sort of flawless logic-computer that only make correct arguments.

hackenslash
In fact, these days, I spend far more effort in correcting these bad arguments than I do arguing with theists

well hackenslash you have an opportunity to correct Ness, please explain to him that those 3 points are correct and uncontroversially true.

I can't wait to see what happens.
1. Either I would be corrected by someone who actually knows what the fuck he is talking about.
2. Or this would backfire and he would correct you on the many mistakes you have made instead.
3. Or both.

In all cases, it is a win win for me.

Just like the probability of both of us being born form the gamete cells of our parents are astronomical. Seriously look up independent assortment and recombinations. That makes any particular genetic combination that result in YOU or ME practically impossible:

well, then why are you making such a big deal with orthologs mutations in chimps and humans and probabilities, ? by you logic my existence is more improbable than similarities between chimps and humans
1 So ether drop that kind of reasoning and admit that it is fallacious
2 or drop common ancestry and your improbability arguments.
please choose 1 or 2.

Still can't figure out the difference between hindsight and foresight.?? Let me explain it once again. The likely hood of you being born before your parents met was extremely unlikely, however since you are now existing being wrong on the internet all the time, the odd of you existing is 100% (sadly enough...joking of course).

The point was to demonstrate that unlikely things happened and continues to happen, as your objection to neutral evolution with your "probabilistic problem".

But again, you missed the point completely. Taking one argument and applying it to something else as if it had the same validity, doesn't work. Saying that the odds of you being born used to be astronomical isn't the same as demonstrating common descent with genetic markers.

The first thing talks about what the odds were for this to have happened, The second thing is noticing the evidence that shows what had happened. Big difference.

ffff, I have gone from A to B to C all the way to Z but you keep demanding more and more such that you can pretend that I have not done anything.

:lol: :lol: :lol: :lol: :lol: :lol: :lol:

no you have not. you have to provide a statistical significan sample (or atleast a single example) of the steps needed to evolve an eye, you haven't done that.

Do I really need to copy paste all those articles.....again....??? That is what I have to put up with when arguing with someone suffering from short term memory.

Origin of opsins[/url]"]
Opsins, and their major divisions (25) arose very early in metazoan evolution. In this article the term ‘opsin’ will refer only to ‘Type 2 animal opsins’, and not to the ‘Type 1 microbial opsins’ of bacteria or the ‘channelrhodopsins’ of algae, both of which are unrelated and appear to have arisen by convergent evolution. The phylogeny of ciliary opsins will be considered in Sections 5 and 6 for chordates generally, and for the vertebrate retina, but for now the questions are: How did the ancestral opsin originate? and What were the initial stages in its diversification?. In addressing these questions, important clues have been obtained through analysis of a number of cnidarian opsin sequences that have become available since 2007 (12, 26-31).

Animal opsins evolved from within the eponymous ‘Rhodopsin family’ of the ‘GRAFS’ superfamily of G-protein coupled receptors (GPCRs), and it is known that this superfamily originated in an ancient eukaryote that existed prior to the divergence of fungi (32)). Recently, Feuda et al (30)) analyzed the phylogeny of opsins and proposed a scheme for the early origin of opsins. They showed that the closest relatives of the opsins are found in the lineage that includes the vertebrate receptors for melatonin. However, for the corresponding GPCRs in invertebrates the ligand has not yet been identified, and so it is not clear what the ancestral ligand might have been at the time that the opsin lineage diverged.

One potential problem with the analysis of Feuda et al (30) is its reliance on the (unproven) existence of R-opsins in cnidaria, but that issue appears to have been resolved by an independent and nearly simultaneous study of opsins from a coral (31), that clearly identified the existence of an R-opsin. The following scenario for the early origin of animal opsins, illustrated in Figure 2B builds on the report of Feuda et al (30), and is presented here as the first in a series of scenarios/hypotheses for the events that gave rise to photoreceptors:

A-1) The forerunner of the first opsin arose through duplication of a GPCR in an ancient metazoan, at a time prior to the divergence of the amoeba-like placozoans.

A-2) That forerunner protein did not possess the retinal-binding lysine (‘K296′) in the seventh transmembrane helix (30); this suggests that retinaldehyde ligand occupied the internal cavity by means of non-covalent binding, as for ligands in conventional GPCRs, and in Figure 2B this pre-opsin is termed a ‘retinaldehyde receptor’. The placozoan Trichoplax has a homolog of opsin (dubbed placopsin by Feuda et al, 2012), that likewise is devoid of the retinal-binding lysine residue.

A-3) Acquisition of an appropriately situated lysine residue within the seventh transmembrane segment of that receptor allowed the retinaldehyde ligand to bind covalently. Initially, the Schiff base bond is likely to have been unprotonated, so that the molecule would have absorbed in the UV. Acquisition of an appropriately located negatively charged residue (e.g. E181) permitted the bond to be protonated, thereby creating the ancestral opsin, and enabling the absorption peak to be shifted into the ‘visible’ spectrum.

A-4) As for most opsins (though not for vertebrate visual opsins), the activated metarhodopsin state of this opsin was thermally stable and could undergo photoreversal to the rhodopsin state. Hence this protein probably did not require a source of 11-cis retinal and could instead utilize all-trans retinal perfectly well.

A-5) Subsequently, two duplications of that earliest opsin occurred, during the relatively short interval between the divergence of placozoa and the divergence of cnidarians from bilaterians. Thus, all of the duplications indicated in Figure 2B took place shortly prior to the first of the numbered branchings shown in Figure 1 (i.e. prior to #1).

an other independent genetic that produces something that connects the cells with the brain, an other independent genetic change that produces a reaction when light is detected.

Figure 2. Origin of opsins, and their possible association with membrane type. A, Opsin phylogeny. Cnidarians have orthologs of each bilaterian opsin subfamily; i.e. the C-, R-, and RGR/Go-opsin subfamilies. Numbers indicate support values (Bayesian PPs) for key nodes. From Feuda et al (2012). B, Hypothesized duplications of ancestral opsin and its precursors, and suggested association with membrane type. An ancient GPCR (related to extant vertebrate melatonin receptors) duplicated, and its ligand became retinaldehyde, which bound non-covalently; this is denoted as ‘Retinaldehyde receptor’. After the divergence of the amoeba-like placozoans (~711 Mya), this GPCR evolved a lysine residue in its seventh transmembrane segment and a negatively charged residue (counterion) so that retinaldehyde bound covalently via a protonated Schiff base linkage; this form is denoted ‘Ancestral opsin’. Within a relatively short interval (prior to the divergence of cnidarians, ~700 Mya), this opsin duplicated twice, giving rise to three major families of opsins: C-opsins, R-opsins, and RGR/Go-opsins. It is proposed that these three opsins preferentially associated with ciliary membrane, microvillar membrane, and the membranes of intracellular organelles, respectively. Note that all these events occurred just prior to the starting point of Fig. 1.

Hypothesized association between opsin type and membrane type . A contributory factor in the co-evolution of opsin classes and photoreceptor classes may have been a preferential association of the different opsins with different regions of membrane, as indicated in Figure 2B. Accordingly, the hypothetical scenario for the early evolution of opsins is extended as follows:

A-6) The two variants of opsin that emerged after the first duplication event may have trafficked preferentially to the membrane of sub-cellular organelles and to surface membrane. Those variants would have given rise to the RGR- division and the C-/R- division, respectively, of modern opsins.

A-7) Following the duplication event that created the distinction between C- and R-opsins, these two variants trafficked to ciliary and microvillar membrane, respectively. In Figure 2B this duplication is shown as having occurred subsequent to the duplication mentioned in the previous point, but at present one cannot reliably distinguish the order in which this pair of duplication events occurred.

A-8) Subsequently, cells expressing the C- and R-opsin classes became distinct from each other, through a process termed ‘division of labor’ (5, 33), leading to (a) ciliary photoreceptors that possessed C-opsins and (b) microvillar photoreceptors that possessed R-opsins; see next Section. The third variant of opsin, RGR-opsin, tended to be expressed in the membranes of intracellular organelles, possibly as an additional opsin in the first two classes of photoreceptors.

A-9) Later in evolution, further division of labor occurred, so that (for example) RGR-opsin could be expressed in separate cells. This would explain how it is possible, on the one hand, for squid photoreceptors to contain an R-opsin in their microvillar membranes as well as retinochrome (an RGR-opsin) in their intracellular organelles, and, on the other hand, for vertebrate cones and rods to contain only a C-opsin in their outer segments whereas RPE cells contain only RGR-opsin in their endoplasmic reticulum.

Metazoan opsin evolution reveals a simple route to animal vision[/url]"]We found that the Placozoa have opsins, and that the opsins share a common ancestor with the melatonin receptors. Further to this, we found that all known neuralian opsins can be classified into the same three subfamilies into which the bilaterian opsins are classified: the ciliary (C), rhabdomeric (R), and go-coupled plus retinochrome, retinal G protein-coupled receptor (Go/RGR) opsins. Our results entail a simple scenario of opsin evolution. The first opsin originated from the duplication of the common ancestor of the melatonin and opsin genes in a eumetazoan (Placozoa plus Neuralia) ancestor, and an inference of its amino acid sequence suggests that this protein might not have been light-sensitive. Two more gene duplications in the ancestral neuralian lineage resulted in the origin of the R, C, and Go/RGR opsins. Accordingly, the first animal with at least a C, an R, and a Go/RGR opsin was a neuralian progenitor.

Synopsis of opsin evolution. This figure represents a gene tree embedded within a species tree illustrating the evolutionary history of the opsins and MLT receptors in Metazoa. It shows that only three duplications and no deletions are necessary to explain opsin evolution.

Evolution of the vertebrate eye: opsins, photoreceptors, retina and eye cup[/url]"]Proposed sequence of events involved in the evolution of the vertebrate eye

Stage 1: bilateral ancestor (>580 million years ago (Mya))

Animals with bilateral symmetry exist2.
Numerous families of genes exist22.
A range of G-protein-coupled signalling cascades exist146.
A primordial opsin has evolved into three major classes: rhabdomeric opsins, photoisomerase-like opsins and ciliary opsins147.
A rhabdomeric-type photoreceptor has evolved, using a Gq-based signalling cascade with a rhabdomeric opsin9.
A ciliary-type photoreceptor has evolved, using a variant opsin (the stem ciliary opsin) that probably coupled to a Go-based signalling cascade8,61,92,148.

~580 Mya
Protostomes separate from our line (deuterostomes).

Stage 2: protochordates (580–550 Mya)

The ciliary photoreceptor and ciliary opsin continue to evolve, becoming similar to those in extant amphioxus and ascidian larvae57,58,62,67.
A primordial RPE65-like isomerase evolves62,65.
These protochordates had ciliary photoreceptors with a ciliary opsin and a hyperpolarizing response, and were able to regenerate 11-cis retinal in darkness.

~550 Mya
Cephalochordates and tunicates separate from our line (chordates).

Stage 3: ancestral craniates (~550–530 Mya)

A ciliary photoreceptor evolves that has well organized outer-segment membranes, an output synapse close to the soma and a synaptic specialization appropriate for graded signal transmission42,86.
Ciliary photoreceptors make synaptic contact onto projection neurons that might have been descendants of rhabdomeric photoreceptors9,69.
The eye-field region of the diencephalon bulges to form lateral ‘eye vesicles’149.
These lateral vesicles invaginate, bringing the proto-retina into apposition with the proto-retinal pigment epithelium149.
A primordial lens placode develops, preventing pigmentation of the overlying skin145.
The resulting paired lateral photoreceptive organs would have resembled the ‘eyes’ of extant hagfish, lacking any image-forming apparatus and subserving non-visual functions.

~530 Mya
Myxiniformes (hagfish) separate from our line (vertebrates).

Stage 4: lamprey-like ancestors (~530–500 Mya)

Photoreceptors develop cone-like features:
- Highly-ordered sac/disc membranes evolve81.
- Mitochondria become concentrated within the ellipsoid region of the inner segment81.
- Coloured filter material is incorporated into the inner segment for spectral tuning83.
- Ribbon synapses evolve in the synaptic terminal78.
- Genome duplications give rise to multiple copies of the phototransduction genes23,24,28,29.
- Cell classes diverge to give five separate cone-like photoreceptors, each with its own ciliary opsin and with isoforms of transduction proteins38,90,93,108.

Retinal computing power increases:
- Cone bipolar cells evolve, either from proto-neurons or from photoreceptors114,150.
- The bipolar cells insert into the pathway from photoreceptors to ganglion cells, through the retraction of photoreceptor processes and the incorporation of new contacts114,126.
- Bi-plexiform ganglion cells develop37.
- A highly organized three-layered neuronal structure with two intervening plexiform layers develops50,51.

Ganglion-cell axons project to the thalamus44,45.
The optics evolve (the lens, accommodation and eye movement):
- The lens placode invaginates and develops to form a lens151.
- The iris develops and a degree of pupillary constriction becomes possible84.
- Innervated extra-ocular muscles evolve152.
The resulting eye and visual system would have resembled that in extant lampreys and would have provided spatial vision at photopic intensities and over a broad wavelength range.

~500 Mya
Petromyzoniformes (lampreys) separate from our line.

Stage 5: jawless fish (~500–430 Mya)

Myelin evolves and is incorporated throughout the nervous system153.
Rod photoreceptors evolve:
- Rhodopsin evolves from cone opsin38,93.
- Rod isoforms of most transduction cascade proteins arise90,108.
- Free-floating discs pinch off within the plasma membrane.
Rod bipolar cells evolve, possibly from rod photoreceptors114.
The scotopic rod pathway evolves, with a new subset of amacrine cells (AII) providing input into the pre-existing cone pathway154,155.
A highly contractile iris evolves that can adjust light levels156.
Intrinsic eye muscles develop that permit accommodation of the lens157.

This eye possessed a duplex retina that contained both rods and cones, together with retinal wiring that closely resembled that of jawed vertebrates, with colour-coded photopic pathways and a dedicated scotopic pathway; it was probably similar to that found in many extant fish.

~430 Mya
The last jawless fish separate from our own line (gnathostomes).

Stage 6: gnathostomes (<430 Mya)

In the case of tetrapods:
- The lens develops an elliptical shape to compensate for the added refractive power that is provided by the cornea in air158.
- The dermal component of the split cornea is lost and the eyelids evolve149.
- Certain opsin classes are lost, for example, SWS2 and Rh2 in mammals, under extended nocturnal conditions159.

Deep homology of eye development and the parallel evolution of animal eyes.[/url]"]

A route for the evolution of photoreceptor cell types and different forms of eyes. a, The cnidarian–bilaterian ancestor had photoreceptors that expressed c-opsin and PAXB. b, Rhabdomeric photoreceptors, r-opsins and PAX6 evolved in ancestral-stem bilaterians, after the split between the cnidarian and bilaterian lineages. c, The last common ancestor of all bilaterians (Urbilateria) probably had two types of light-sensing organ: a prototypical eye and a brain photo-clock, which are both found in the annelid Platynereis dumerilii. d, The photoreceptor types established in the Urbilateria were then incorporated in different ways in the parallel evolution of different eyes in various phyla. Rhabdomeric photoreceptors were the foundation for the evolution of compound and camera-type eyes in arthropods and molluscs, respectively. Both types of photoreceptor were incorporated into the vertebrate eye, with ciliary receptors carrying out phototransduction and rhabdomeric receptors being transformed into ganglion cells and functioning in image processing. Pigment cells are not shown. e, The ciliary camera-type eyes of box jellyfish are also proposed to have evolved in parallel in the cnidarian lineage. f, Cladogram depicting the evolutionary relationships of the taxa shown in a–e. (Panels a–e courtesy of L. Olds (University of Wisconsin, Madison); panel f courtesy of K. Monoyios (University of Chicago, Illinois).)

Flexibly deployed Pax genes in eye development at the early evolution of animals demonstrated by studies on a hydrozoan jellyfish[/url]"]

In our present model, gene duplications that gave rise to distinct subfamilies occurred most likely before the separation of poriferans and eumetazoans (1 in Fig. 5), as suggested by the statistical tests in refs. 4 and 22. We cannot, however, completely eliminate the possibility that some (or all) of these duplications postdate the poriferans–eumetazoans split (dashed line in Fig. 5) (4) until more sponge Pax genes that do not belong to the Pax-2/5/8 subfamily are found. When the ancestral animal eye evolved in the common ancestor of cnidarians and bilaterians, Pax genes may have been recruited as components of the gene network responsible for eye development (2 in Fig. 5). We assume that, at this stage, several classes (corresponding to subfamilies) of Pax genes were redundantly involved in this network. After the divergence of bilaterians and cnidarians on one hand, and hydrozoans and cubozoans on the other hand, the three distinct animal lineages selected different classes of Pax genes for the roles in eye development and/or maintenance (3 in Fig. 5). Such molecular-level opportunism is often observed in evolution (e.g., lens crystallins) (47). Interestingly, formation of some bilaterian eyes seems to be Pax-6 independent (ref. 14 for review). This suggests that the gene network directing eye development can be anomalously modified, making Pax-6 dispensable for eye development in some bilaterian lineages (4 in Fig. 5).

Cephalopod eye evolution was modulated by the acquisition of Pax-6 splicing variants[/url]"]
Acquisition of the Pax-6 variants in eye formation

As found in several bilaterian species, the basic function of animal Pax-6 appears to involve the regulation of the anterior part of the head and the initiation of photoreceptor formation, regardless of the photoreceptor cell type. In insect Pax-6, ey has at least three additional variants generated through gene duplication. The duplicates are thought to have originated in a pancrustacean ancestor (insect + crustacea), although the exact origin remains uncertain9. The roles of two of these duplicates, toy and eyg, have diverged in the compound eye formation processes of the fly and beetle27,28, and functional changes in toy and eyg have significantly contributed to the evolution of the size and shape of the eyes in the beetle27. These results indicate that the diversification of the Pax6 isoforms by duplication is required for eye development in insects. Diversification of Pax-6 variants is also found in vertebrates. However, the acquisition of variations in Pax-6 is completely distinct between these two taxa; vertebrate Pax-6(5a) originated from the alternative splicing of the locus, whereas insect eyg originated from gene duplication29. Pax-6(5a) shows functional similarity to the Drosophila eyg, which also lacks the PD required for HD function30. In mice, another type of protein variation, protein sumoylation onto the Pax-6 splicing variants, is expressed in the embryonic optic and lens vesicles and shows different DNA-binding and transcriptional activities from the authentic protein3. The bilaterian common ancestor (UBA) is considered to have had a Pax-6 gene for the development of photoreceptors (Figure 4). Thus, eye development has been achieved by alternative splicing or gene duplication, either of which leads to variations in the protein isoforms.

Evolution of crystallins for a role in the vertebrate eye lens[/url]"]
The camera eye lens of vertebrates is a classic example of the re-engineering of existing protein components to fashion a new device. The bulk of the lens is formed from proteins belonging to two superfamilies, the α-crystallins and the βγ-crystallins. Tracing their ancestry may throw light on the origin of the optics of the lens. The α-crystallins belong to the ubiquitous small heat shock proteins family that plays a protective role in cellular homeostasis. They form enormous polydisperse oligomers that challenge modern biophysical methods to uncover the molecular basis of their assembly structure and chaperone-like protein binding function. It is argued that a molecular phenotype of a dynamic assembly suits a chaperone function as well as a structural role in the eye lens where the constraint of preventing protein condensation is paramount. The main cellular partners of α-crystallins, the β- and γ-crystallins, have largely been lost from the animal kingdom but the superfamily is hugely expanded in the vertebrate eye lens. Their structures show how a simple Greek key motif can evolve rapidly to form a complex array of monomers and oligomers. Apart from remaining transparent, a major role of the partnership of α-crystallins with β- and γ-crystallins in the lens is to form a refractive index gradient. Here, we show some of the structural and genetic features of these two protein superfamilies that enable the rapid creation of different assembly states, to match the rapidly changing optical needs among the various vertebrates.

I already told you what I mean by step.

Well what i would call a step requires 3 things
1 a genetic change achievable in 1 generation (like a gene duplication for example)
2 it has to be beneficial (something that would be selected by natural selection)
3 it has to represent a step closer towards modern eyes

Addressed it:

Why would it have to be achievable in 1 generation? Why not 2, or 5, or a hundred? The answer is that it doesn't.
Why would it have to be "positive" rather than neutral? It doesn't. It could even be slightly deleterious and still fix by drift in a small population, or substantially deleterious yet hitchike with another beneficial allele.
Why would someone have to provide a step by step path at this level of detail? Do you even have any other beliefs which are supported by such a level corroboration? Of course you don't.
Isn't it obvious you're deliberately setting the bar irrationally high? Yes, yes it is.
......................
No. I'm obviously not claiming all of eye-evolution was achieved by genetic drift, that would be preposterous. Rather, I'm merely saying that not all of the "steps" have to be beneficial. We know for a fact that there are complex phenotypes who's evolutionary history include necessary neutral mutations that fixed by genetic drift.
For example, the evolution of chloroquine resistance in plasmodium falciparum requires multiple neutral mutations along the way.
And in the Long-Term Evolution Experiment, the cit+ phenotype requires at least one neutral, potentiating mutation.

each change (or at least most of them) would have to be beneficial

This is simply not true, and the fact that it isn't true has been pointed out six ways from Sunday.
You're operating from an entirely false premise. Not only are they not required to be beneficial, they're not even required to be beneficial in the context of their environment. There's no sense in which your contention isn't fundamentally wrong.

And you admitted that requirement #2 isn't necessary.

granted, not all of the steps have to be beneficial.

So why include that requirement again? Suffer from short term memory? From looking at old discussions between you and others and from my own experience by arguing with you, I think you do.
You frequently bring up points back even though they have been refuted before, like that Bat/Dolphin echolocation thing that you brought back some time later after I have shown that to be flawed. Stop using PRATTS.

My question is which of these mechanisms predominated
1 neutral mutation + genetic drift
2 beneficial mutation + selection

second time I ask the question and second time that you did not answer,

I did answer, though you probably didn't see it when I was still editing my post.

Here it is:::

So please answer this question, any objection that I might have depends on how you answer this question.
talking about the evolution of sight...........are you a neutralist or a selectionist?

Both. Since there are so many neutral mutation (some that do lead to changes in phenotypes) that get inherited, genetic drift has been proven to be a larger role in the evolution of species. Does that mean natural selection played no role? No, it still does.

nice try, so your strategy is to keep your answer ambiguous, because you know that neutralism has a probabilistic problem that you cant solve, and selectionism has a burden proof that you don't what to carry, namely identify the mutations that could have occurred and prove that they had a benefit.

1. No I said BOTH, that is not ambiguous. Natural selection and genetic drift are NOT mutually exclusive mechanisms in the sense of no 100% this or 100% that. They can both contribute to the fixation or elimination of mutations in a population with varying degrees depending on the population size. Stop thinking in black or white.
2. Neutralism doesn't have a probabilistic problem as I have already explained. There are extremely unlikely events like us being born if you calculated it as if with foresight, but that is the problem. We note this things in hindsight, thus it doesn't matter how likely the event that happened could happen. Once it happened, the odds of it happening are 100%.

"That a particular specified event or coincidence will occur is very unlikely. That some astonishing unspecified events will occur is certain. That is why remarkable coincidences are noted in hindsight, not predicted with foresight."
—David G. Myers

My question is which of these mechanisms predominated
1 neutral mutation + genetic drift
2 beneficial mutation + selection
I know that you believe that both mechanisms took place, my question is which of these 2 mechanisms predominated in the evolution of eyes.
lets see how long does it take you to answer this question clearly and ambiguously.....or you can simply admit that you don't know .....

You don't have to wait long, since I already have answered that question, though not clearly. I said this

Both. Since there are so many neutral mutation (some that do lead to changes in phenotypes) that get inherited, genetic drift has been proven to be a larger role in the evolution of species. Does that mean natural selection played no role? No, it still does.

So drift dominates mostly during evolution of species, especially when the population size is small, which it often is. So you might think that the way life evolved in this particular way is very unlikely, you would be right. If you rewind the tape to about 1 billion years ago and let everything play out on its own, chances are that familiar species won't ever evolve. You would still have bacteria and maybe even eukaryotes if they already existed 1 billion years ago, however there would be other things that would be unrecognizable. Maybe similar in the same way a dolphin is similar to a shark or a bat is to a bird, but you won't find anything that you could say that is a mammal or a bird. Just like if you rewind the tape back before you were a zygote, when you mom and dad had that very special night, changes are that a different sperm cell fertilized the egg, so instead of you being born, a different human being equivalent to your brother or sister would have been born which was FAAARRR more likely.

But again, there is a different in noticing improbable events in foresight and hindsight.

(END repeat)

Your supposed answer.

So drift dominates mostly during evolution of species, especially when the population size is small, which it often is. So you might think that the way life evolved in this particular way is very unlikely, you would be right. If you rewind the tape to about 1 billion years ago and let everything play out on its own, chances are that familiar species won't ever evolve. You would still have bacteria and maybe even eukaryotes if they already existed 1 billion years ago, however there would be other things that would be unrecognizable. Maybe similar in the same way a dolphin is similar to a shark or a bat is to a bird, but you won't find anything that you could say that is a mammal or a bird. Just like if you rewind the tape back before you were a zygote, when you mom and dad had that very special night, changes are that a different sperm cell fertilized the egg, so instead of you being born, a different human being equivalent to your brother or sister would have been born which was FAAARRR more likely.

We are not talking about mutations in general, we are talking about the specific mutations responsable of evolving the eye (human eye for example) where this mutations mainly neutral or beneficial? ....which mutations predominated in the evolution of the human eye?............(or feel free to use some other eye)

So I did answer your question, then why tell me I didn't? And I already did answer that. Drift mostly dominates in evolution, especially when population sizes are small. Read the whole response before you come back again with this bogus "probability problem" of yours.

Using an argument and replacing certain words to make a parody only works when you use it in the correct context that is applicable. Otherwise it will make you look like an idiot.

"According to the multi verse theory, there are many universes and some have conditions that allow for humans to pick there noses. And since this observation can only exists within a universe with specific conditions that allows humans pick their nose, it is not a surprise that we find ourselves in a universe with those conditions. It is a tautology really and that is it."

What you keep missing is that the argument applies to conditions that allows humans to LIVE.
There is no indication that we must live in a universe with specific conditions that allows us to pick our noses thus there is no reason that should find ourselves in such a universe, and there is no indication that we should find ourselves within a universe where all life shares genetic markers that indicate common ancestry....if we are somehow not related. This last part you omitted from your parody, because that demonstrates why the parody is so dumb.

in fact the parody and the analogy is valid.

No it is not and the parts that are written as this explains why.

according to the multiverse hypothesis, there are universes where chimps and humans have orthologues mutations, simply by chance.
given that we live in a universe where we observe those similarities, it obvious that we live in such universe.

However, there is no reason why we should live in such universe, unlike living in a universe that allows us to live. Thus the multiverse argument for why we live in such a universe cannot be used to argue why we live in a universe where we share genetic orthologs with other species.
There is a missing part in your argument, WHY should we live in such a universe??

I have spelled this out many different way, how many times do I have to tell you this again before you leave for a while and come back with the same thing??

observers that can observe themselves in a universe where chimps and humans have orthologues mutations can only exist in universes where they have such orthologs mutations.

this is analogous to.....

observers that observe themselves living in a universe can only exist in a universe where they can exist and make such observations.

Wrong.

To make it analogous.

1. Observers can only exists in a universe that allows for them to live, otherwise they wouldn't exists in the first place (correct multi verse argument)

2. Observers can only exists in a universe that includes them sharing orthologs with other species, otherwise they wouldn't exists in the first place (premise one is false, observes don't need to have shared orthologs with other species in order for them to exists....IF they are unrelated to other species, thus the multiverse argument doesn't apply here)

 

[Nesslig20]

How do I delete a reply?

 

[Nesslig20]

Not spotted anything yet.

Say Hackenslash, what do you think about this?

Rumraket wrote:
Some atheistic arguments, or responses, are in fact stupid and silly. I have no compunction agreeing to that. I'm an atheist yet it is entirely obvious to me that some atheists are atheists for bad reasons, or have no, or bad answers to some theistic arguments. In becoming an atheist, one does not magically transform into some sort of flawless logic-computer that only make correct arguments.

hackenslash
In fact, these days, I spend far more effort in correcting these bad arguments than I do arguing with theists

well hackenslash you have an opportunity to correct Ness, please explain to him that those 3 points are correct and uncontroversially true.

I can't wait to see what happens.
1. Either I would be corrected by someone who actually knows what the fuck he is talking about.
2. Or this would backfire and he would correct you on the many mistakes you have made instead.
3. Or both.

In all cases, it is a win win for me.

Those 3 points are these below with my response to each of them.

1Accepting Common Ancestry and our current phylogenetic tree, implies that bats and dolphins suffered from the same mutations in the same loci 200 independent times
http://www.nature.com/nature/journal/v502/n7470/full/nature12511.html

There is no such thing as "suffering" from a mutation, unless the mutation is harmful, which of course these weren't. The article noted that of the 805,053 amino acids within 2,326 orthologous coding gene sequences only 200 were found to be convergent. That is not very big considering the vast data they had to sift through. Also the mutations didn't have to be identical since different mutations can result in the same amino-acid sequences, which is what they looked at. They didn't look at genetic sequences, they looked at amino-acid sequences.

For example, a missense mutations that changes the codon
AAU to ACU
would change the amino acid from Asn to Thr.

And if you change the codon GCU to ACU
it would change the amino acid from Ala to Thr.

Different codons changed by different mutations to into still different codons, but resulting in the same amino acid being translated.

I and others have already explained this too.

2 There is no current explanation on how could 2 independent clades could have sufferer form the same mutations 200 independent times, even assuming strong selective pressure, it is very unlikely for 2 organisms to have the same random mutation in the same place. (let alone 200)

Very unlikely as in 200 out of 805,053 (0,024%) of the time, which don't need to be identical mutations.

3 evolution (common ancestry) predicted that similarities in echolocation would have been superficial (like wings in bats and birds) similarities where not expected at a genetic level.

Correction, similarities were not expected at the protein/amino acid level, since they looked at the amino acid sequence, not the genetic sequence. And even if it was a surprise, now we see that amino acids substitutions can happen independently 200 out of 805053 times between lineages that diverged hundreds of thousands of generations ago.

Surprises doesn't mean, the whole theory is wrong or the theory is incorrect in part. A new exciting discovery was made that no one expected, but the results didn't contradicted anything. Among other surprises the article showed is that many of the genes linked to vision showed convergence as well, meaning that vision could be linked to echolocation, but that surprise doesn't show that anybody was wrong about vision or echolocation.

none of this disproves common ancestry, it simply proves that there are some missing pieces in the puzzle.

If the puzzle was your brain and the missing pieces was the cognitive ability to listen to the same answers that were given a thousand times before.

What do you say, are you now going to explain to me that those three points are in fact "correct AND uncontroversially true"?

 

[Deleted member 619]

I can't wait to see what happens.
1. Either I would be corrected by someone who actually knows what the fuck he is talking about.
2. Or this would backfire and he would correct you on the many mistakes you have made instead.
3. Or both.

In all cases, it is a win win for me.

What's most interesting to me is that leroy cites a paper from the evolutionary primary literature as if it supports anything other than evolution.

Yes, it's interesting that we got an unexpected result. Does it turn over evolutionary theory? Not remotely, it provides a greater understanding of evolution. This is entirely to be expected, because evolution is a fact.

The literature is replete with examples of convergent evolution. This is a not expected example of the scale on which this can occur, with entire sequences being converged on. Is this a problem for evolution? No, because only evolution provides an explanation and, while not expected on this scale, it's entirely in line with evolutionary theory.

This is just like the soft tissue example. We thought it couldn't survive, but we were wrong, and now we know better, because we've found an example. This doesn't make evolutionary theory wrong, and it doesn't lack an evolutionary explanation, it merely shows that we haven't gotten all the details yet.

Backfire it is.

 

[he_who_is_nobody]

How do I delete a reply?

When you hit Edit, above the Post Icons there is a box and next to it, it says "Once deleted the post cannot be recovered". I have never used it, so I am not sure what one needs to do after that.