Study find 100's of possible alternative evolutionary paths

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Study find 100's of possible alternative evolutionary paths

#1  Postby Shrunk » Sep 16, 2017 12:27 pm

More important work from Joe Thornton's lab:

Scientists at the University of Chicago studied a massive set of genetic variants of an ancient protein, discovering a myriad of other ways that evolution could have turned out and revealing a central role for chance in evolutionary history.

The study, published this week in Nature by University of Chicago graduate student Tyler Starr and his advisor Professor Joseph Thornton, is the first to subject reconstructed ancestral proteins to deep mutational scanning—a state-of-the-art technique for characterizing massive libraries of protein variants. The authors' strategy allowed them to compare the path that evolution actually took in the deep past to the millions of alternative routes that could have been taken, but were not.

Starting with a resurrected version of an ancient protein that evolved a new function some 500 million years ago - a function critical to human biology today—the researchers synthesized a massive library of genetic variants and used deep mutational scanning to analyze their functions. They found more than 800 different ways that the protein could have evolved to carry out the new function as well, or better than, the one that evolved historically.

https://phys.org/news/2017-09-scientist ... e.html#jCp


Can't wait to see what the ID creationists have to say about this.

Original paper (behind a pay wall) here:

http://www.nature.com/nature/journal/va ... lback=true
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Re: Study find 100's of possible alternative evolutionary paths

#2  Postby Rumraket » Sep 16, 2017 8:48 pm

Ancestral sequence reconstruction really does utterly refute ID-creationism.
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Re: Study find 100's of possible alternative evolutionary paths

#3  Postby Wortfish » Sep 17, 2017 11:21 am

Rumraket wrote:Ancestral sequence reconstruction really does utterly refute ID-creationism.


No. ID proponents and creationists both accept that microevolution occurs, especially at the molecular level. The paper doesn't address the origin of the protein, a transcription factor, but rather small changes in its specificity over time.
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Re: Study find 100's of possible alternative evolutionary paths

#4  Postby Zadocfish2 » Sep 17, 2017 11:44 pm

Wortfish wrote:
Rumraket wrote:Ancestral sequence reconstruction really does utterly refute ID-creationism.


No. ID proponents and creationists both accept that microevolution occurs, especially at the molecular level. The paper doesn't address the origin of the protein, a transcription factor, but rather small changes in its specificity over time.


"Microevolution" isn't a thing, though, that's what ID proponents don't seem to get no matter how often it's explained to them. It's a single force, just seen on different timescales. If you accept microevolution, you lock yourself into either believing in evolution or believing in YEC.
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Re: Study find 100's of possible alternative evolutionary paths

#5  Postby Greyman » Sep 18, 2017 2:24 am

Shrunk wrote:Can't wait to see what the ID creationists have to say about this.
They'll pretend that the evolution of a new function is "just a small change to specificity", then shift the goalposts to claim that they've always been okay with incremental development of proteins, but that many small steps can not lead to big steps.
Wortfish wrote:
Rumraket wrote:Ancestral sequence reconstruction really does utterly refute ID-creationism.

No. ID proponents and creationists both accept that microevolution occurs, especially at the molecular level. The paper doesn't address the origin of the protein, a transcription factor, but rather small changes in its specificity over time.
To the contrary, prominent IDcreation proponentists have espoused that the one true sequence of amino acids needed to produce a specific new function could not have arisen through pure chance.
Last edited by Greyman on Sep 18, 2017 2:28 am, edited 1 time in total.
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Re: Study find 100's of possible alternative evolutionary paths

#6  Postby Just A Theory » Sep 18, 2017 2:26 am

Wortfish wrote:
Rumraket wrote:Ancestral sequence reconstruction really does utterly refute ID-creationism.


No. ID proponents and creationists both accept that microevolution occurs, especially at the molecular level. The paper doesn't address the origin of the protein, a transcription factor, but rather small changes in its specificity over time.


That's what I love about science. For every question that is answered, two more are raised!

Keep up the good work Wortfish :thumbup: :clap: :dance:
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Re: Study find 100's of possible alternative evolutionary paths

#7  Postby Rumraket » Sep 18, 2017 8:33 am

Wortfish wrote:
Rumraket wrote:Ancestral sequence reconstruction really does utterly refute ID-creationism.


No. ID proponents and creationists both accept that microevolution occurs, especially at the molecular level.

There are so many things wrong with your response one hardly knows where to even begin.

First of all, the evolutionary history of a single protein is neither a micro or macroevolutionary event. It can be associated with both, in that the protein can change as the carrying species evolve, diverge and undergo speciation and large-scale morphological change. Or the species can remain relatively morphologically static while it undergoes slow genomic change. Both things are possible and neither are necessarily associated with the evolutionary history of a protein.

Second, in this particular case, the evolutionary history of the protein in question stretches back over 450 million years and even predates the origin of vertebrates. There has been quite a lot of diversification and macroevolution going on for the species that carry orthologoues of it. Aka all of sexually reproducing vertebrates.
To emphasize the point: It would not be POSSIBLE to reconstruct the evolutionary history of this protein if MACROEVOLUTION did not take place. We are talking about the origin and diversification of ALL OF VERTEBRATES as the platform for the diversifiction and evolution of this single protein.

To make it even clearer, here are some examples of the diverging nature of vertebrates:
Image

Third, creationists and ID proponents VEHEMENTLY reject ALL sorts of "blind" evolution (microevolutionary or otherwise). Creationist in particular are taught to stay away from the word 'evolution' entirely. They're taught to call all instances of microevolution (such as the evolution of antibiotic resistance in microbes) for 'adaptation' rather than evolution, and to insist it is just "a pre-existing ability to adapt".

ID-Creationists of all stripes pay lip-service to the idea that they accept microevolution, as a rhetorical device, yet in actual fact they utterly reject it. They have all sorts of practiced and rehearsed responses, such as "the information for adaptation was front-loaded/pre-programmed into the genomes and just had to activate first". So no, they don't accept microevolution. They claim they do, they utter the words like you just did "we accept microvoluiton", but in actual fact they don't. They LIE when they say they do.

The paper doesn't address the origin of the protein, a transcription factor, but rather small changes in its specificity over time.

Straighforwardly false.

Fist of all, the paper DOES address the origin and diverging evolutionary histories of two entire classes of transcription factors, from a single ancestor >450 million years ago. And by what standard of measure is the change in specificity from the ancestor, "small"? That's just denialist rhetoric. They prefer DNA sequences that diverge by 33%. How is that a "small" change?

The proteins themselves from their respective classes, differ from each other by as much as ~80% of their total amino acids.
The SR protein from Sheep (Q95L13_SHEEP from UniPROT), has an amino acid sequence identity of 19.4% to the orthologous SR protein from american alligators (Q765N5_ALLMI from UniPROT). You can even find this protein in Octopus, an invertebrate. The Octopus protein (Q765N5_ALLMI, UniPROT) has a sequence identity to the American Alligator protein of only 15%. This is so divergent if those were the only two proteins you had, you couldn't infer a homologous relationship without structure-functional data. Then we'd have someone like you sit here and claim they would be entirely different proteins and couldn't possibly have a common evolutionary source.
But that massive divergence can be bridged, incrementally, through the orthologous proteins spread out in the diversity of life. So you're fucked.

In the words of the authors:
Starr et al 2017 wrote:We applied deep mutational scanning to the DNA-binding domain of a reconstructed ancestral steroid hormone receptor, whose historical trajectory of functional, genetic, and biochemical evolution is well understood. Steroid receptors are transcription factors that mediate the action of sex and adrenal steroids by binding to specific DNA sequences and regulating expression of target genes. The two major clades of receptors differ in their DNA specificity (Fig. 1a): oestrogen receptors prefer an inverted palindrome of AGGTCA (oestrogen response element, ERE)(13), whereas receptors for androgens, progestogens, and corticosteroids prefer AGAACA (steroid response element, SRE)(14). Although some degeneracy is tolerated, these sequences represent the high-affinity consensus sites for each class(13,14) and have therefore been the focus of extensive biochemical characterization(15–18). Previously, we reconstructed the ancestral protein from which all steroid receptors descend (AncSR1) and found that it specifically binds ERE(11,12). After AncSR1 duplicated, one daughter protein diverged in function to yield AncSR2, which prefers SRE. Re-introducing three substitutions from this historical interval radically shifts the relative affinity of AncSR1 from ERE to SRE, and this effect is robust to uncertainty about the ancestral sequence(19).

My bolds.

So what you, random internet nobody, call a "rather small cange in specificity", the authors of the paper call a radical shift in affinity.

Second, there used to be only one protein, and now there is two, so one had to actually originate. It originated by duplication and they both subsequently diverged. Furthermore, the study in question PROVES that besides the massive changes in protein sequence and function that has taken place over the last 450 million years of macroevolutionary change, there were STILL MANY MANY MORE functional evolutionary trajectories possible.

This thing, the whole thing, in this single paper, properly understood and looked at in context, ROYALLY FUCKS UP THE ASS all IDcreationist arguments ever. Ever.
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Re: Study find 100's of possible alternative evolutionary paths

#8  Postby theropod » Sep 18, 2017 12:22 pm

:this:

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Re: Study find 100's of possible alternative evolutionary paths

#9  Postby Shrunk » Sep 18, 2017 1:00 pm

Greyman wrote:
Wortfish wrote:
Rumraket wrote:Ancestral sequence reconstruction really does utterly refute ID-creationism.

No. ID proponents and creationists both accept that microevolution occurs, especially at the molecular level. The paper doesn't address the origin of the protein, a transcription factor, but rather small changes in its specificity over time.
To the contrary, prominent IDcreation proponentists have espoused that the one true sequence of amino acids needed to produce a specific new function could not have arisen through pure chance.


Yes. Specifically, this was claimed by Douglas Axe here:

https://www.ncbi.nlm.nih.gov/pubmed/15321723

Those claims were pretty solidly refuted by Arthur Hunt in an article at Panda's Thumb. But this current article goes a step further and actually correctly calculates the number of functional proteins (of a specific function) that exist in sequence space, the very thing Axe tried (and failed) to determine.

This is in addition to number of empirical studies that have been reviewed by Rumraket which already showed Axe's figures were too low, by as many a 60 orders of magnitude. :what:

The magnitude of the defeat this presents for ID cannot be overstated. Axe's figures on "protein folds" is one of the chief premises of Stephen Meyer's entire argument in "Darwin's Doubt", so on this one issue alone that entire book's argument collapses (although it fails in many, many other ways besides.) And Axe's study is repeatedly trotted out as a rare instance of peer reviewed studies which supposedly support ID (which would not be true even if Axe had got his numbers right.)

So they have to respond to this paper. But they can't without lying. Which is OK, because that's what they're good at.
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Re: Study find 100's of possible alternative evolutionary paths

#10  Postby Just A Theory » Sep 18, 2017 11:57 pm

Rumraket wrote:Stuff.


Sorry Rumraket, but none of this addresses the fact that microevolution only occurs within created kinds.

QED.

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Re: Study find 100's of possible alternative evolutionary paths

#11  Postby Wortfish » Sep 19, 2017 12:33 pm

Rumraket wrote:
There are so many things wrong with your response one hardly knows where to even begin. First of all, the evolutionary history of a single protein is neither a micro or macroevolutionary event. It can be associated with both, in that the protein can change as the carrying species evolve, diverge and undergo speciation and large-scale morphological change. Or the species can remain relatively morphologically static while it undergoes slow genomic change. Both things are possible and neither are necessarily associated with the evolutionary history of a protein.

This paper is not reporting large-scale morphological changes, only changes to hormone receptors.

Second, in this particular case, the evolutionary history of the protein in question stretches back over 450 million years and even predates the origin of vertebrates. There has been quite a lot of diversification and macroevolution going on for the species that carry orthologoues of it. Aka all of sexually reproducing vertebrates.
To emphasize the point: It would not be POSSIBLE to reconstruct the evolutionary history of this protein if MACROEVOLUTION did not take place. We are talking about the origin and diversification of ALL OF VERTEBRATES as the platform for the diversifiction and evolution of this single protein.

Macroevolution, strictly understood as "speciation" or "adaptive radiation", is not disputed by either creationists or ID proponents. There is also the possibility, not considered by the authors, that some parallel or convergent evolution has taken place, which does not involve common ancestry.

Third, creationists and ID proponents VEHEMENTLY reject ALL sorts of "blind" evolution (microevolutionary or otherwise). Creationist in particular are taught to stay away from the word 'evolution' entirely. They're taught to call all instances of microevolution (such as the evolution of antibiotic resistance in microbes) for 'adaptation' rather than evolution, and to insist it is just "a pre-existing ability to adapt".

That's just semantics. Creationists accept that mutations occur and that some loss-of-function mutations can be beneficial.

ID-Creationists of all stripes pay lip-service to the idea that they accept microevolution, as a rhetorical device, yet in actual fact they utterly reject it. They have all sorts of practiced and rehearsed responses, such as "the information for adaptation was front-loaded/pre-programmed into the genomes and just had to activate first". So no, they don't accept microevolution. They claim they do, they utter the words like you just did "we accept microvoluiton", but in actual fact they don't. They LIE when they say they do.

No. There isn't a single creationist who, for example, denies that bacteria adapt to their environment through mutations: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3708842/

Fist of all, the paper DOES address the origin and diverging evolutionary histories of two entire classes of transcription factors, from a single ancestor >450 million years ago. And by what standard of measure is the change in specificity from the ancestor, "small"? That's just denialist rhetoric. They prefer DNA sequences that diverge by 33%. How is that a "small" change?

No. It talks about descent from an ancestral gene/protein, and associated changes, not the origin of the ancestor itself.

The proteins themselves from their respective classes, differ from each other by as much as ~80% of their total amino acids. The SR protein from Sheep (Q95L13_SHEEP from UniPROT), has an amino acid sequence identity of 19.4% to the orthologous SR protein from american alligators (Q765N5_ALLMI from UniPROT). You can even find this protein in Octopus, an invertebrate. The Octopus protein (Q765N5_ALLMI, UniPROT) has a sequence identity to the American Alligator protein of only 15%. This is so divergent if those were the only two proteins you had, you couldn't infer a homologous relationship without structure-functional data. Then we'd have someone like you sit here and claim they would be entirely different proteins and couldn't possibly have a common evolutionary source. But that massive divergence can be bridged, incrementally, through the orthologous proteins spread out in the diversity of life. So you're fucked.


The SR protein for sheep you cite is an estrogen alpha receptor. A BLAST between the human and the chicken for ESR1 shows a 79% identity, not the low levels you report:

Code: Select all
[b]Score   Expect   Method   Identities   Positives   Gaps[/b]
964 bits(2491)    0.0    Compositional matrix adjust.    463/589(79%)    516/589(87%)    7/589(1%)

Query  1    MTMTLHTKASGVTLLHQIQGTELETLSRPQLKIPLERSLSDMYVESNKTGVFNYPEGATY  60
            MTMTLHTKASG+ LLHQIQG ELE L+RPQLKIPLER L ++Y++S+K  V+NYPEGA Y
Sbjct  1    MTMTLHTKASGMALLHQIQGNELEPLNRPQLKIPLERPLGEVYLDSSKPAVYNYPEGAAY  60

Query  61   DFGTTAP----VYGSTTLSYAPTSES--FGSSSLAGFHSLNNVPPSPVVFLQTAPQLSPF  114
            +F   A     VYG T L Y P SE+  FGS+ L GF  LN+V PSP++ L   PQLSPF
Sbjct  61   EFNAAAAANAQVYGQTGLPYGPGSEAAAFGSNGLGGFPPLNSVSPSPLMLLHPPPQLSPF  120

Query  115  IHHHSQQVPYYLENEQGSFGMREAAPPAFYRPSSDNRRHSIRERMSSTNEKGSLSMESTK  174
            +  H QQVPYYLENE   + +REA PPAFYRP+SDNRR   RER++STN+KGS++MES K
Sbjct  121  LQPHGQQVPYYLENEPSGYTVREAGPPAFYRPNSDNRRQGGRERLASTNDKGSMAMESAK  180

Query  175  ETRYCAVCNDYASGYHYGVWSCEGCKAFFKRSIQGHNDYMCPATNQCTIDKNRRKSCQAC  234
            ETRYCAVCNDYASGYHYGVWSCEGCKAFFKRSIQGHNDYMCPATNQCTIDKNRRKSCQAC
Sbjct  181  ETRYCAVCNDYASGYHYGVWSCEGCKAFFKRSIQGHNDYMCPATNQCTIDKNRRKSCQAC  240

Query  235  RLRKCYEVGMMKGGIRKDRRGGEMMKQKRQREEQDSRNGEASSTELRAPTLWTSPLVVKH  294
            RLRKCYEVGMMKGGIRKDRRGG M+K KRQR++ + R    S+ ++RA  LW SPL++K
Sbjct  241  RLRKCYEVGMMKGGIRKDRRGGRMLKHKRQRDDGEGRGEVGSAGDMRAANLWPSPLMIKR  300

Query  295  NKKNSPALSLTAEQMVSALLEAEPPIVYSEYDPNRPFNEASMMTLLTNLADRELVHMINW  354
            +KKNS ALSLTA+QMVSALL+AEPPI+YSEYDP RPF+EASMM LLTNLADRELVHMINW
Sbjct  301  SKKNSLALSLTADQMVSALLDAEPPILYSEYDPTRPFSEASMMGLLTNLADRELVHMINW  360

Query  355  AKRVPGFVDLTLHDQVHLLECAWLEILMIGLVWRSMEHPGKLLFAPNLLLDRNQGKCVEG  414
            AKRVPGFVDLTLHDQVHLLECAWLEILMIGLVWRSMEHPGKLLFAPNLLLDRNQGKCVEG
Sbjct  361  AKRVPGFVDLTLHDQVHLLECAWLEILMIGLVWRSMEHPGKLLFAPNLLLDRNQGKCVEG  420

Query  415  MVEIFDMLLATAARFRMMNLQGEEFVCLKSIILLNSGVYTFLSSTLKSLEERDYIHRVLD  474
            MVEIFDMLLAT++RFRMMNLQGEEFVCLKSIILLNSGVYTFLSSTLKSLEE+D+IHRVLD
Sbjct  421  MVEIFDMLLATSSRFRMMNLQGEEFVCLKSIILLNSGVYTFLSSTLKSLEEKDHIHRVLD  480

Query  475  KITDTLIHLMAKSGLSLQQQHRRLAQLLLILSHIRHMSNKGMEHLYNMKCKNVVPLYDLL  534
            KITDTLIHLMAK+GL+LQQQH+RLAQLLLILSHIRHMSNKGMEHLY+MKCKNVVPLYDLL
Sbjct  481  KITDTLIHLMAKAGLTLQQQHQRLAQLLLILSHIRHMSNKGMEHLYSMKCKNVVPLYDLL  540

Query  535  LEMLDAHRLHAPAARSAAPMEEENRNQLTTAPA-SSHSLQSFYINSKEE  582
            LEMLDAHRLHAP +R  A +EE +++ L TA + SSHSLQ +YI  + E
Sbjct  541  LEMLDAHRLHAPTSRGGASVEETDQSHLATAGSTSSHSLQKYYITGEAE  589


But you were comparing an ER for sheep with a PR (progesterone) receptor for the alligator. Apples and oranges.

In the words of the authors:
Starr et al 2017 wrote:We applied deep mutational scanning to the DNA-binding domain of a reconstructed ancestral steroid hormone receptor, whose historical trajectory of functional, genetic, and biochemical evolution is well understood. Steroid receptors are transcription factors that mediate the action of sex and adrenal steroids by binding to specific DNA sequences and regulating expression of target genes. The two major clades of receptors differ in their DNA specificity (Fig. 1a): oestrogen receptors prefer an inverted palindrome of AGGTCA (oestrogen response element, ERE)(13), whereas receptors for androgens, progestogens, and corticosteroids prefer AGAACA (steroid response element, SRE)(14). Although some degeneracy is tolerated, these sequences represent the high-affinity consensus sites for each class(13,14) and have therefore been the focus of extensive biochemical characterization(15–18). Previously, we reconstructed the ancestral protein from which all steroid receptors descend (AncSR1) and found that it specifically binds ERE(11,12). After AncSR1 duplicated, one daughter protein diverged in function to yield AncSR2, which prefers SRE. Re-introducing three substitutions from this historical interval radically shifts the relative affinity of AncSR1 from ERE to SRE, and this effect is robust to uncertainty about the ancestral sequence(19).

My bolds.


The authors seem to be making the case that the small changes to the daughter gene - three substitutions to be precise - act as a sort of switch between estrogen and androgen specificity. I presume that both androgens and estrogens were produced in the ancestors of vertebrates, so it isn't clear to me if this is an innovation or just a separation of existing functions/specificities.

So what you, random internet nobody, call a "rather small cange in specificity", the authors of the paper call a radical shift in affinity.Second, there used to be only one protein, and now there is two, so one had to actually originate. It originated by duplication and they both subsequently diverged. Furthermore, the study in question PROVES that besides the massive changes in protein sequence and function that has taken place over the last 450 million years of macroevolutionary change, there were STILL MANY MANY MORE functional evolutionary trajectories possible. This thing, the whole thing, in this single paper, properly understood and looked at in context, ROYALLY FUCKS UP THE ASS all IDcreationist arguments ever. Ever.

They can describe it as "radical", but they need to be able to quanitfy what they mean by this. As you point out, a copy of an ancestral gene has evolved - through three small changes - differing binding affinity but it is not clear if these mutations simply disabled the ability of the duplicate gene to bind with estrogen-specific DNA sequences. The ancestral gene may have been, as the authors state, "promiscuous". And, of course, it is highly doubtful that all steroid receptors are descended from this hypothetical reconstruction which is more of a template than an actual ancestor.
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Re: Study find 100's of possible alternative evolutionary paths

#12  Postby DavidMcC » Sep 19, 2017 3:53 pm

"Wortfish wrote:Macroevolution, strictly understood as "speciation" or "adaptive radiation", is not disputed by either creationists or ID proponents. There is also the possibility, not considered by the authors, that some parallel or convergent evolution has taken place, which does not involve common ancestry.


I suppose you think that it requires a god to cause convergent or parallel evolution. :roll:
Most of us would go with similarity of specific selective factors.
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Re: Study find 100's of possible alternative evolutionary paths

#13  Postby Shrunk » Sep 19, 2017 4:16 pm

wortfish wrote:There is also the possibility, not considered by the authors, that some parallel or convergent evolution has taken place, which does not involve common ancestry.


What results would you predict from this study if that were the case? Would they still be able to determine the structure of a common ancestral protein, and the mutational paths taken to the present day proteins? How would convergent evolution mitigate their main finding of multiple pathways thru sequence space by which functional proteins can be realized?
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Re: Study find 100's of possible alternative evolutionary paths

#14  Postby Rumraket » Sep 19, 2017 4:46 pm

Wortfish wrote:This paper is not reporting large-scale morphological changes, only changes to hormone receptors.

I know. Which is why I wrote that you bringing up the terms micro and macroevolution to begin with was besides the point.

Wortfish wrote:Macroevolution, strictly understood as "speciation" or "adaptive radiation", is not disputed by either creationists or ID proponents.

Total bullshit.

Wortfish wrote:
Rumraket wrote:Third, creationists and ID proponents VEHEMENTLY reject ALL sorts of "blind" evolution (microevolutionary or otherwise). Creationist in particular are taught to stay away from the word 'evolution' entirely. They're taught to call all instances of microevolution (such as the evolution of antibiotic resistance in microbes) for 'adaptation' rather than evolution, and to insist it is just "a pre-existing ability to adapt".

That's just semantics. Creationists accept that mutations occur and that some loss-of-function mutations can be beneficial.

I agree that creationist arguments are just semantics. So too is the labeling of mutations as "loss-of-function" mutation. Just semantics. Actually it's nothing but a rhetorical trick.

Wortfish wrote:
Rumraket wrote:ID-Creationists of all stripes pay lip-service to the idea that they accept microevolution, as a rhetorical device, yet in actual fact they utterly reject it. They have all sorts of practiced and rehearsed responses, such as "the information for adaptation was front-loaded/pre-programmed into the genomes and just had to activate first". So no, they don't accept microevolution. They claim they do, they utter the words like you just did "we accept microvoluiton", but in actual fact they don't. They LIE when they say they do.

No. There isn't a single creationist who, for example, denies that bacteria adapt to their environment through mutations: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3708842/

Yes there are, we've had some on this site. I've argued with these nutcases before myself. There was one over on talkrational who outright denied that adaptation had anything to do with mutation. And this isn't an unusual phenomenon. I suggest you go to the well-known pro ID blogs like uncommon descent and ask "what kind of evidence is there really that mutations and selection can produce any kind of adaptation?". Then notice how nobody actually answers that question but instead join you in the implication that there is no such evidence. Why would they do that? Because they completely reject all the evidence for anything evolution related. Including the adaptive power of mutation. They're so nuts they think the concep of fitness itself is incoherent and they reject that natural selection takes place. I'm not kidding you.

Wortfish wrote:
Rumraket wrote:Fist of all, the paper DOES address the origin and diverging evolutionary histories of two entire classes of transcription factors, from a single ancestor >450 million years ago. And by what standard of measure is the change in specificity from the ancestor, "small"? That's just denialist rhetoric. They prefer DNA sequences that diverge by 33%. How is that a "small" change?

No. It talks about descent from an ancestral gene/protein, and associated changes, not the origin of the ancestor itself.

I don't claim it addresses the origin of the ancestor itself, so there's nothing to say "no" to.

Wortfish wrote:
Rumraket wrote:The proteins themselves from their respective classes, differ from each other by as much as ~80% of their total amino acids. The SR protein from Sheep (Q95L13_SHEEP from UniPROT), has an amino acid sequence identity of 19.4% to the orthologous SR protein from american alligators (Q765N5_ALLMI from UniPROT). You can even find this protein in Octopus, an invertebrate. The Octopus protein (Q765N5_ALLMI, UniPROT) has a sequence identity to the American Alligator protein of only 15%. This is so divergent if those were the only two proteins you had, you couldn't infer a homologous relationship without structure-functional data. Then we'd have someone like you sit here and claim they would be entirely different proteins and couldn't possibly have a common evolutionary source. But that massive divergence can be bridged, incrementally, through the orthologous proteins spread out in the diversity of life. So you're fucked.

The SR protein for sheep you cite is an estrogen alpha receptor.

Yes that was a typo, one is an SR and another is an ER. The comparison is still valid however.

Wortfish wrote:A BLAST between the human and the chicken for ESR1 shows a 79% identity, not the low levels you report:

The numbers I report are absolutely correct, but notice how I wrote "as much as ~80%". I didn't say all of them diverge exactly as much. Which should have been obvious since I cite two different numbers for two different comparisons. They were examples I picked from their supplementary materials files where they list all the proteins they used to infer ancestral states with.
Obviously the closer related the species are, the less time there will have been for differences to accumulate. Sheep and Humans are both mammals, and therefore their proteins are much more similar, and for the same class of receptors (SR only) the differences will also be smaller. Octopus is an invertebrate, and is therefore among the most divergent from the vertebrates, and of course much more divergent than the level of differences you will get from within mammals.

Wortfish wrote:But you were comparing an ER for sheep with a PR (progesterone) receptor for the alligator. Apples and oranges.

No, they have a common ancestor protein, which was an ER, that's the point.
Steroid receptors (SR) arose from oestrogen receptors (ER) over 450 million years ago.

But I see now that what you called "a rather small change in the specificity of a transcription factor" up above, you're now calling "apples and oranges". Hoisted by your own petard!

Wortfish wrote:The authors seem to be making the case that the small changes to the daughter gene - three substitutions to be precise - act as a sort of switch between estrogen and androgen specificity. I presume that both androgens and estrogens were produced in the ancestors of vertebrates, so it isn't clear to me if this is an innovation or just a separation of existing functions/specificities.

What they find is that it only takes three specific amino acid substitutions for the functional switch to occur in a duplicate of the ancestral oestrogen receptor (AncSR1), in order to produce the ancestral steroid receptor (AncSR2). The proteins have been further drifting apart ever since.


Wortfish wrote:
Rumraket wrote:So what you, random internet nobody, call a "rather small cange in specificity", the authors of the paper call a radical shift in affinity.Second, there used to be only one protein, and now there is two, so one had to actually originate. It originated by duplication and they both subsequently diverged. Furthermore, the study in question PROVES that besides the massive changes in protein sequence and function that has taken place over the last 450 million years of macroevolutionary change, there were STILL MANY MANY MORE functional evolutionary trajectories possible. This thing, the whole thing, in this single paper, properly understood and looked at in context, ROYALLY FUCKS UP THE ASS all IDcreationist arguments ever. Ever.

They can describe it as "radical", but they need to be able to quanitfy what they mean by this.

Funny how the need to make quantifiable statements about the size of the functional shift is now suddenly a requirement when the rhetoric is turned back against you.

But they actually explain that the SR no longer interacts with the ERE (oestrogen response element, AGGTCA), and ER no longer interacts with SRE (steroid response element, AGAACA). They can no longer perform each other's functions. And the ancestral protein AncSR1 that gave rise to both classes (SR and ER) preferred ERE exclusively. So the function for interacting with SRE came after duplication and divergence of the two copies.

Wortfish wrote:As you point out, a copy of an ancestral gene has evolved - through three small changes - differing binding affinity but it is not clear if these mutations simply disabled the ability of the duplicate gene to bind with estrogen-specific DNA sequences.

It is not clear from the small part I quoted above, and the specific work was elucidated in a previous publication of theirs from 2014:

McKeown AN, Bridgham JT, Anderson DW, Murphy MN, Ortlund EA, Thornton JW.
Evolution of DNA specificity in a transcription factor family produced a new gene regulatory module.
Cell. 2014 Sep 25;159(1):58-68. doi: 10.1016/j.cell.2014.09.003

In that paper there's this nice figure:
Fig1.jpg
Fig1.jpg (132.33 KiB) Viewed 348 times

Accompanied by this text:
Figure 1. Evolution of Novel Specificity Occurred via a Discrete Shift
between AncSR1 and AncSR2
(A) Architecture of SR response elements. All SRs bind to an inverted palindrome of two half-sites (gray arrows) separated by variable bases (n). x indicates sites at which ERE and SREs differ.
(B) SR phylogeny comprises two major clades, which have nonoverlapping specificity for ligands (stars) and REs (boxes). Preferred half-sites for each clade are shown; bases that differ are underlined. Ancestral and extant receptors are colored by RE specificity (purple, ERE; green, SREs; pink, extended monomeric ERE). The orange box indicates evolution of specificity for SREs; number of substitutions on this branch and the total number of DBD residues are indicated. Nodal support is marked by the approximate likelihood ratio statistic (aLRS): unlabeled, aLRS 1 to 10; one solid dot indicates aLRS 10 to 100; two solid dots indicate aLRS > 100. Scale bar is in substitutions per site.
(C) AncSR1 specifically activates reporter gene expression driven by ERE (purple bar) with no activation from SRE1 (light green) or SRE2 (dark green); AncSR2’s specificity is distinct. Bar height indicates fold activation relative to vector-only control with SEM of three experimental replicates.
(D) Ancestral binding affinities reflect distinct specificities for ERE versus SREs. Bars heights indicate the macroscopic affinity (KA,mac) of binding to palindromic DNA response elements, measured using fluorescence polarization; error bars show SEM of three experimental replicates. Colors as in (C).
(E–G) The components of macroscopic binding affinity—affinity for a half-site (K1) and cooperativity of binding (u)—by AncSR1 and AncSR2 were estimated by easuring binding to a half-site and a full palindromic RE and then globally fitting the data to a model containing both parameters. Error bars show SEM of three experimental replicates. See Figure S1 and Tables S1, S2, and S3.

I have highlighted the relevant part in bold.

Wortfish wrote:The ancestral gene may have been, as the authors state, "promiscuous".

They don't write that, where do you get this crap from?

They explicitly reject that inference:
McKeown et al 2014 wrote:The distinct specificities of extant SRs could have evolved by partitioning the activities of a promiscuous ancestor among descendants or by a discrete switch from ancestral to derived forms of specificity. To distinguish among these possibilities, we synthesized coding sequences for the inferred ancestral DBDs and characterized their functions and physical properties. We focused on the capacity to bind ERE, SRE1, and SRE2 because these classical REs differ only at two bases in the half-site and are fully distinct in their responses to the two classes of SR (Zilliacus et al., 1992). Using a dual luciferase reporter assay in cultured cells (Figure 1C), we found that AncSR1 had DNA specificity like that of extant ERs, driving strong activation from ERE but exhibiting no expression above background from SREs. AncSR2, in contrast, specifically activated from both SREs but did not activate from ERE. These results are consistent with the strong sequence similarity between AncSR1 and extant ERs and between AncSR2 and the vertebrate ARs, PRs, GRs, and MRs (Figure 1B). They are further corroborated by the pattern of RE specificities across extant members of the SR family tree: because all known descendants of AncSR2 recognize SREs and all other family members and close outgroups bind ERE-like sequences, the most parsimonious expectation by far is SRE specificity by AncSR2 and ERE specificity by AncSR1 (Eick and Thornton, 2011).


Wortfish wrote:And, of course, it is highly doubtful that all steroid receptors are descended from this hypothetical reconstruction which is more of a template than an actual ancestor.

Thank you for this pile of counterfactual assertions, all of which are contradicted by the results of these papers. Basically what you just did amounts to saying "nya nya didn't happen". :lol:
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Re: Study find 100's of possible alternative evolutionary paths

#15  Postby Rumraket » Sep 19, 2017 5:58 pm

I see I also made another typo. The Octopus protein is called Q19AB0_OCTVU in UniPROT.

It's an estrogen receptor. And alignment between the Octopus ER, and Human ER-Beta gives this result:
Identity: 26.207%
Code: Select all
CLUSTAL O(1.2.4) multiple sequence alignment

TR|Q19AB0|Q19AB0_OCTVU -----------------------------------MIDKQV-------TAADDIKMLSPD 18
SP|Q92731|ESR2_HUMAN   MDIKNSPSSLNSPSSYNCSQSILPLEHGSIYIPSSYVDSHHEYPAMTFYSPAVMNYSIPS 60
                                                           :*.:         :   ::   *.

TR|Q19AB0|Q19AB0_OCTVU RCAHIHGSTGHAATAASSSSGHSATTSSSTTTSSSTSSSSSSSSSSSSSSSSSSANPQTP 78
SP|Q92731|ESR2_HUMAN   NVTNLEGGPGRQTTS---------------------------------------PNVLWP 81
                       . :::.*. *: :*:                                        *   *

TR|Q19AB0|Q19AB0_OCTVU TSTTL-------EMADMQT----AGESGGVQLATTVAGD-TALLTTDFKKKYDSVVAGSS 126
SP|Q92731|ESR2_HUMAN   TPGHLSPLVVHRQLSHLYAEPQKSPWCEARSLEHTLPVNRETLKRKVSGNRCASPVTGPG 141
                       *   *       :::.: :    :  . . .*  *:  :  :*  .   ::  * *:* .

TR|Q19AB0|Q19AB0_OCTVU TGNTTRLCQVCDDNASGFHYGVWSCEGCKAFFKRSIQGPVDYVCPATNSCTIDKHRRKSC 186
SP|Q92731|ESR2_HUMAN   SKRDAHFCAVCSDYASGYHYGVWSCEGCKAFFKRSIQGHNDYICPATNQCTIDKNRRKSC 201
                       : . :::* **.* ***:********************  **:*****.*****:*****

TR|Q19AB0|Q19AB0_OCTVU QACRLRKCYEVGMNKGSQRKERKNSSNQTKVKRSSADFSDSTV-NSTSGNQPAKSQRLSK 245
SP|Q92731|ESR2_HUMAN   QACRLRKCYEVGMVKCGSRRERCGYRLVRRQRSADEQLHCAGKAKRSGGHAPRVRE---- 257
                       ************* * ..*:** .     : : :. ::  :   : :.*: *   :   

TR|Q19AB0|Q19AB0_OCTVU SSSLVEELSKNDFAV-------P-ECKLNPSIPLTKNYILQLLIQVADKDLVQLINWAKH 297
SP|Q92731|ESR2_HUMAN   --LLLDALSPEQLVLTLLEAEPPHVLISRPSAPFTEASMMMSLTKLADKELVHMISWAKK 315
                          *:: ** :::.:       *     .** *:*:  ::  * ::***:**::*.***:

TR|Q19AB0|Q19AB0_OCTVU IPGYADLSLSDQVHLIECCWMELVLLNCAYRSMEYEGKRLAFASNLILEKHHW-EILGMT 356
SP|Q92731|ESR2_HUMAN   IPGFVELSLFDQVRLLESCWMEVLMMGLMWRSIDHPGKL-IFAPDLVLDRDEGKCVEGIL 374
                       ***:.:*** ***:*:*.****::::.  :**::: **   ** :*:*::..   : *:

TR|Q19AB0|Q19AB0_OCTVU QILEQVAAVSEQLLQFGINREELLLLEATILVNAEVRRLAGFSKIDDIRQ---IILNALI 413
SP|Q92731|ESR2_HUMAN   EIFDMLLATTSRFRELKLQHKEYLCVKAMILLNSSMYPLVTATQDADSSRKLAHLLNAVT 434
                       :*:: : *.:.:: :: ::::* * ::* **:*:.:  *.  ::  *  :    :***:

TR|Q19AB0|Q19AB0_OCTVU D-------TAQKYHPDNPRHVPSALLLLSHVRQASDRSIIYLQKQKDEGHVTFCELITEM 466
SP|Q92731|ESR2_HUMAN   DALVWVIAKSGISSQQQSMRLANLLMLLSHVRHASNKGMEHLLNMKCKNVVPVYDLLLEM 494
                       *       .:     ::  :: . *:******:**::.: :* : * :. * . :*: **

TR|Q19AB0|Q19AB0_OCTVU LEAQNSSNDIVAPRADVIGMGT------------------ 488
SP|Q92731|ESR2_HUMAN   LNAHVLRGC----KSSITGSECSPAEDSKSKEGSQNPQSQ 530
                       *:*:   .     ::.: *                     


Another alignment, this time between the Human ER-Beta and Human Glucocorticoid (SR) receptor:
Identity: 15.689%
Clearly the oestrogen receptors are more diverget from the steroid receptors, than the oestrogen receptors are from each other.
Code: Select all
CLUSTAL O(1.2.4) multiple sequence alignment

SP|Q92731|ESR2_HUMAN ------------------------------------------------------------
SP|P04150|GCR_HUMAN  MDSKESLTPGREENPSSVLAQERGDVMDFYKTLRGGATVKVSASSPSLAVASQSDSKQRR 60
                                                                                 

SP|Q92731|ESR2_HUMAN ------------------------------------------------------------
SP|P04150|GCR_HUMAN  LLVDFPKGSVSNAQQPDLSKAVSLSMGLYMGETETKVMGNDLGFPQQGQISLSSGETDLK 120
                                                                                 

SP|Q92731|ESR2_HUMAN ------------------------------------------------------------
SP|P04150|GCR_HUMAN  LLEESIANLNRSTSVPENPKSSASTAVSAAPTEKEFPKTHSDVSSEQQHLKGQTGTNGGN 180
                                                                                 

SP|Q92731|ESR2_HUMAN -----------------------------------------------MDIKNSPSSLNSP 13
SP|P04150|GCR_HUMAN  VKLYTTDQSTFDILQDLEFSSGSPGKETNESPWRSDLLIDENCLLSPLAGEDDSFLLEGN 240
                                                                    :  ::.   *:.

SP|Q92731|ESR2_HUMAN SSYNCSQSILPL-------------------------------------------EHGSI 30
SP|P04150|GCR_HUMAN  SNEDCKPLILPDTKPKIKDNGDLVLSSPSNVTLPQVKTEKEDFIELCTPGVIKQEKLGTV 300
                     *. :*.  ***                                            : *::

SP|Q92731|ESR2_HUMAN YIPSSYVDSHHEYPAMTFYSPAVMNYSIPSNVTNLEGGPGRQTTSPN-------VLWPTP 83
SP|P04150|GCR_HUMAN  YCQASFPG-------ANIIGNKMSAISVH--GVSTSGGQMYHYDMNTASLSQQQDQKPIF 351
                     *  :*: .        .: .  :   *:    .. .**   :    .          * 

SP|Q92731|ESR2_HUMAN GHLSPLVVHRQLSHLYAEPQKSPWCEARS--LEHTLPVNRE-TLKRKVSGNRCASPV--- 137
SP|P04150|GCR_HUMAN  NVIPPIPV-----------GSENWNRCQGSGDDNLTSLGTLNFPGRTVFSNGYSSPSMRP 400
                     . : *: *            .. * ..:.   ::   :.      *.* .*  :**   

SP|Q92731|ESR2_HUMAN ---------TGPGSKRDAHFCAVCSDYASGYHYGVWSCEGCKAFFKRSIQGHNDYICPAT 188
SP|P04150|GCR_HUMAN  DVSSPPSSSSTATTGPPPKLCLVCSDEASGCHYGVLTCGSCKVFFKRAVEGQHNYLCAGR 460
                              :   :    ::* **** *** **** :* .**.****:::*:::*:* .

SP|Q92731|ESR2_HUMAN NQCTIDKNRRKSCQACRLRKCYEVGMVKCGSRRERCGYRLVRRQRSADEQLHCAGKAKRS 248
SP|P04150|GCR_HUMAN  NDCIIDKIRRKNCPACRYRKCLQAGMNLEARKTKKKIKGI-QQ--------ATTGVSQE- 510
                     *:* *** ***.* *** *** :.**   . : ::    : ::          :* ::.

SP|Q92731|ESR2_HUMAN GGHAPRVREL---LLDALSPEQLVLTLLEAEPPHVLISR--PSAPFTEASMMMSLTKLAD 303
SP|P04150|GCR_HUMAN  TSENPGNKTIVPATLPQLTP--TLVSLLEVIEPEVLYAGYDSSVPDSTWRIMTTLNMLGG 568
                      .. *  : :    *  *:*   :::***.  *.** :    *.* :   :* :*. *..

SP|Q92731|ESR2_HUMAN KELVHMISWAKKIPGFVELSLFDQVRLLESCWMEVLMMGLMWRSIDHP--GKLIFAPDLV 361
SP|P04150|GCR_HUMAN  RQVIAAVKWAKAIPGFRNLHLDDQMTLLQYSWMFLMAFALGWRSYRQSSANLLCFAPDLI 628
                     ::::  :.*** **** :* * **: **: .** :: :.* ***  :   . * *****:

SP|Q92731|ESR2_HUMAN LDRDEGKCVEGILEIFDMLLATTSRFRELKLQHKEYLCVKAMILLNSSMYPLVTATQDAD 421
SP|P04150|GCR_HUMAN  INEQRMT-LPCMYDQCKHMLYVSSELHRLQVSYEEYLCMKTLLLLSSVPKDGLKSQELFD 687
                     ::.:. . :  : :  . :* .:*.::.*::.::****:*:::**.*     :.: :  *

SP|Q92731|ESR2_HUMAN SSRKLAHLLNAVTDALVWVIAKSGISSQQQSMRLANLLMLLSHVRHASNKGMEHLLNMKC 481
SP|P04150|GCR_HUMAN  EIR-M-TYIKELGKA---IVKREGNSSQ-NWQRFYQLTKLLDSM----HEVVENLLNYCF 737
                     . * :   :: : .*   :: :.* *** :  *: :*  **. :    :: :*:***   

SP|Q92731|ESR2_HUMAN KNV------VPVYDLLLEMLNAHVLRGCKSSITGSECSPAEDSKSKEGSQNPQSQ 530
SP|P04150|GCR_HUMAN  QTFLDKTMSIEFPEMLAEIITNQIPKYSNGNIKKLLFH----QK----------- 777
                     :..      : . ::* *::. :: : .:..*.         .*           
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Re: Study find 100's of possible alternative evolutionary paths

#16  Postby Wortfish » Sep 19, 2017 6:30 pm

Rumraket wrote:
Wortfish wrote:Macroevolution, strictly understood as "speciation" or "adaptive radiation", is not disputed by either creationists or ID proponents.

Total bullshit.


Poorly-informed anti-creationist scoffers occasionally think they will ‘floor’ creation apologists with examples of ‘new species forming’ in nature. They are often surprised at the reaction they get from the better-informed creationists, namely that the creation model depends heavily on speciation.It seems clear that some of the groupings above species (for example, genera, and sometimes higher up the hierarchy) are almost certainly linked by common ancestry, that is, are the descendants of one created ancestral population (the created kind, or baramin).

https://creation.com/speciation-confere ... eationists

I agree that creationist arguments are just semantics. So too is the labeling of mutations as "loss-of-function" mutation. Just semantics. Actually it's nothing but a rhetorical trick.

So why do many scientists talk about such mutations?
Loss-of-function mutations in SLC30A8 protect against type 2 diabetes:
http://www.nature.com/ng/journal/v46/n4 ... .2915.html

Yes there are, we've had some on this site. I've argued with these nutcases before myself. There was one over on talkrational who outright denied that adaptation had anything to do with mutation. And this isn't an unusual phenomenon. I suggest you go to the well-known pro ID blogs like uncommon descent and ask "what kind of evidence is there really that mutations and selection can produce any kind of adaptation?". Then notice how nobody actually answers that question but instead join you in the implication that there is no such evidence. Why would they do that? Because they completely reject all the evidence for anything evolution related. Including the adaptive power of mutation. They're so nuts they think the concep of fitness itself is incoherent and they reject that natural selection takes place. I'm not kidding you.

In some cases, already existing variation - rather than new mutations - allows adaptation to occur, right? :scratch:

I don't claim it addresses the origin of the ancestor itself, so there's nothing to say "no" to.

Agreed. So we misunderstood each other.

Yes that was a typo, one is an SR and another is an ER. The comparison is still valid however.

Estrogen receptors (ERs) are a type of SR (steriod receptor).

The numbers I report are absolutely correct, but notice how I wrote "as much as ~80%". I didn't say all of them diverge exactly as much. Which should have been obvious since I cite two different numbers for two different comparisons. They were examples I picked from their supplementary materials files where they list all the proteins they used to infer ancestral states with. Obviously the closer related the species are, the less time there will have been for differences to accumulate. Sheep and Humans are both mammals, and therefore their proteins are much more similar, and for the same class of receptors (SR only) the differences will also be smaller. Octopus is an invertebrate, and is therefore among the most divergent from the vertebrates, and of course much more divergent than the level of differences you will get from within mammals.

My objection is that you weren't comparing the same gene in different species, but rather different genes (though still steroid receptors) in different species. Humans and chickens, my example, are almost as far apart as sheep and alligators.

No, they have a common ancestor protein, which was an ER, that's the point.
Steroid receptors (SR) arose from oestrogen receptors (ER) over 450 million years ago.

What the authors claim is that steroid response - for hormones other than estrogen - can be traced back to AncSR2, the duplicate copy of AncSR1. Estrogen receptor capability appears to have been the default.

But I see now that what you called "a rather small change in the specificity of a transcription factor" up above, you're now calling "apples and oranges". Hoisted by your own petard!

According to the authors, it was a small change, resulting in a shift in binding affinity.

What they find is that it only takes three specific amino acid substitutions for the functional switch to occur in a duplicate of the ancestral oestrogen receptor (AncSR1), in order to produce the ancestral steroid receptor (AncSR2). The proteins have been further drifting apart ever since.

Just to remind you, estrogen is a steroid hormone. There are other steroids, such as androgens, that the authors claim were not part of the receptor capability of AncSR1, but they also acknowledge that the ancestor was "promiscuous" in function. That makes me suspect it may have had dual-functionality and didn't discriminate between steroids, although it was much more specific to estrogen than other steroids. Androgens exist in the zebrafish and, indeed, in most chordates.

Funny how the need to make quantifiable statements about the size of the functional shift is now suddenly a requirement when the rhetoric is turned back against you.

Quantification helps when making radical claims, if you excuse the pun.

But they actually explain that the SR no longer interacts with the ERE (oestrogen response element, AGGTCA), and ER no longer interacts with SRE (steroid response element, AGAACA). They can no longer perform each other's functions. And the ancestral protein AncSR1 that gave rise to both classes (SR and ER) preferred ERE exclusively. So the function for interacting with SRE came after duplication and divergence of the two copies.

That is true. But how could the ancestral protein prefer ERE *exclusively* when, presumably, there were other steroid hormones produced in the organism that had this ancestral gene? Were there no males in the population?

My other point is that the paper only reconstructs the ligand-binding capability of all steroid receptors. It doesn't account for the fact that this class of transcription factor diverge greatly in ways that are not related with DNA binding affinity.

They don't write that, where do you get this crap from?

Evolution of Minimal Specificity and Promiscuity in Steroid Hormone Receptors: http://journals.plos.org/plosgenetics/a ... en.1003072
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Re: Study find 100's of possible alternative evolutionary paths

#17  Postby Shrunk » Sep 19, 2017 7:18 pm

It's so embarrassing to watch someone metaphorically shit their own bedclothes like this. Why do you keep humiliating yourself, Wortfish?
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Re: Study find 100's of possible alternative evolutionary paths

#18  Postby Wortfish » Sep 19, 2017 7:55 pm

Shrunk wrote:It's so embarrassing to watch someone metaphorically shit their own bedclothes like this. Why do you keep humiliating yourself, Wortfish?

At least I know that estrogen is a steroid hormone. So is it not possible for anyone to criticise a scientific paper and the interpretation that arises from it?
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Re: Study find 100's of possible alternative evolutionary paths

#19  Postby Rumraket » Sep 19, 2017 8:19 pm

Wortfish wrote:
Rumraket wrote:
Wortfish wrote:Macroevolution, strictly understood as "speciation" or "adaptive radiation", is not disputed by either creationists or ID proponents.

Total bullshit.


Poorly-informed anti-creationist scoffers occasionally think they will ‘floor’ creation apologists with examples of ‘new species forming’ in nature. They are often surprised at the reaction they get from the better-informed creationists, namely that the creation model depends heavily on speciation. It seems clear that some of the groupings above species (for example, genera, and sometimes higher up the hierarchy) are almost certainly linked by common ancestry, that is, are the descendants of one created ancestral population (the created kind, or baramin).

https://creation.com/speciation-confere ... eationists

So there are creationists who accept speciation, and creationists that don't. I'll note the irony of creationists accepting that nesting hiearchies are evidence for common ancestry within some arbitrarily defined clade, yet at the same time reject it is evidence for common ancestry at greater levels. Why? Nobody knows.

Regardless, here is a list of examples of creationists either not accepting speciation, or somehow trying to make it appear as if it has nothing to do with evolution:
https://evolutionnews.org/2017/04/two-genetic-blows-against-darwinian-speciation/
"Two Genetic Blows Against Darwinian Speciation"
This one's so bad it's almost unreadable. The jargon and rhetorical devices are everywhere.
evolutionnews wrote:Classical neo-Darwinism relies on genetic mutations (random mistakes) acted on by natural selection (an aimless effect dependent on what survives). From these two sources of unguided happenstance, all the adapted perfections in life are supposed to have emerged. But what if life is, instead, determined by active information content? An entirely different picture of evolutionary change becomes possible: one that involves information sharing. Two recent genomic studies provide additional validation for the new picture.

...


https://evolutionnews.org/2012/01/does_the_eviden/
"Does the Evidence for Speciation Come from Nature or Groupthink?"

https://uncommondescent.com/intelligent-design/speciation-more-new-species-discovered-really/
"Speciation: More new species discovered – really?"

https://uncommondescent.com/intelligent-design/science-news-release-admits-evidence-for-speciation-implicit-in-charles-darwins-work-is-scarce/
"Science news release admits evidence for speciation “implicit in Charles Darwin’s work” is scarce"

https://www.discovery.org/a/18121
"Specious Speciation: The Myth of Observed Large-Scale Evolutionary Change"

Here's one from answers in genesis where they try to claim speciation isn't evolution. Which is of course ridiculous, since speciation counts as macroevolution. Which... is evolution.
https://answersingenesis.org/kids/science/speciation-evolution/
Notice all the silly rhetorical devices in that last article, which is one big attempt to diminish the fact that speciation is an evolutionary event. For example: "The formation of a new species generally results in a loss of genetic information—the opposite type of change required by molecules-to-man evolution. As two populations of the same created kind become separated, genetic variation is diminished, resulting in the formation of a new species."

That is a perfect example of what I describe below, that creationists will always call mutations loss of function (or loss of information). Somehow they just have to find some way to make it appear as if none of it can be evidence for evolution. All of it is just clever rhetoric. Suddenly evolution is too fast, and this is a problem for evolution. Or evolution is too slow, and species remain static, and this is also a problem for evolution. And there's no new genetic information, it was all "front-loaded" or "pre-existing". And so on and so forth.

I agree that creationist arguments are just semantics. So too is the labeling of mutations as "loss-of-function" mutation. Just semantics. Actually it's nothing but a rhetorical trick.

So why do many scientists talk about such mutations?
Loss-of-function mutations in SLC30A8 protect against type 2 diabetes:
http://www.nature.com/ng/journal/v46/n4 ... .2915.html

There is such a thing as loss of function mutations. That isn't the issue.

The issue is that creationists always call mutations loss of function mutations. The creationist MO is that it doesn't matter what kind of mutation it is, or what effect it has, since there will in some sense always be something that is replaced with something else. The creationist will then emphasize the replacement by calling it a loss, and ignore the gain.

If there's switch in a function, from one type of reaction catalyzed, to another similar but not identical reaction catalyzed, then creationists will insist on emphasizing how the two reactions are similar, so as to try to rhetorically diminish the evidence.

A DNA binding protein became an enzyme instead? Well then it lost the DNA binding capability, so loss of function. A protein that catalyzed one class of reactions, changed and catalyzed another? Then it lost the other one, so loss of function. A promiscous ancestor diverged into several distinct classes? Then the descendants individually lost lots of functions. THAT is how their rhetoric works.

Yes there are, we've had some on this site. I've argued with these nutcases before myself. There was one over on talkrational who outright denied that adaptation had anything to do with mutation. And this isn't an unusual phenomenon. I suggest you go to the well-known pro ID blogs like uncommon descent and ask "what kind of evidence is there really that mutations and selection can produce any kind of adaptation?". Then notice how nobody actually answers that question but instead join you in the implication that there is no such evidence. Why would they do that? Because they completely reject all the evidence for anything evolution related. Including the adaptive power of mutation. They're so nuts they think the concep of fitness itself is incoherent and they reject that natural selection takes place. I'm not kidding you.

In some cases, already existing variation - rather than new mutations - allows adaptation to occur, right? :scratch:

And there we have it, that's the very kind of behavior I talk about.

That's just more rhetoric. How did that existing variation come to exist in the first place? By mutation. But because we weren't around to see those mutations arise, creationists will insist they didn't, and just call it pre-existing variation. Which is just more rhetoric.

Yes that was a typo, one is an SR and another is an ER. The comparison is still valid however.

Estrogen receptors (ERs) are a type of SR (steriod receptor).

For a broader definition of steroid. But the authors define a steroid receptor as a receptor for androgens, progestogens, and
corticosteroids. So they distinguish between what they call oestrogen receptors, and steroid receptors, though yes technically they're both steroids. Regardless, all of them evolved from the same ancestral protein, which they have reconstructed and they call AncSR1, which existed before the origin of vertebrates.

The numbers I report are absolutely correct, but notice how I wrote "as much as ~80%". I didn't say all of them diverge exactly as much. Which should have been obvious since I cite two different numbers for two different comparisons. They were examples I picked from their supplementary materials files where they list all the proteins they used to infer ancestral states with. Obviously the closer related the species are, the less time there will have been for differences to accumulate. Sheep and Humans are both mammals, and therefore their proteins are much more similar, and for the same class of receptors (SR only) the differences will also be smaller. Octopus is an invertebrate, and is therefore among the most divergent from the vertebrates, and of course much more divergent than the level of differences you will get from within mammals.

My objection is that you weren't comparing the same gene in different species, but rather different genes (though still steroid receptors) in different species. Humans and chickens, my example, are almost as far apart as sheep and alligators.

I understood your objection and I explained why it was meaningless to make it.

All steroid receptors, for oestrogens, androgens, progestogens, retinoids, and corticosteroids, evolved from the same ancestral protein. So my comparison of two arbitrarily picked steroid receptors from different species, to highlight how much these proteins have changed in amino acid sequence over time, is still valid.

No, they have a common ancestor protein, which was an ER, that's the point.
Steroid receptors (SR) arose from oestrogen receptors (ER) over 450 million years ago.

What the authors claim is that steroid response - for hormones other than estrogen - can be traced back to AncSR2, the duplicate copy of AncSR1. Estrogen receptor capability appears to have been the default.

Yes, so my comparison is entirely valid.

But I see now that what you called "a rather small change in the specificity of a transcription factor" up above, you're now calling "apples and oranges". Hoisted by your own petard!

According to the authors, it was a small change, resulting in a shift in binding affinity.

Really? Quote them then. I can't find that anywhere in the 2017 or 2014 papers that have been cited here. So where do you get this?

What they find is that it only takes three specific amino acid substitutions for the functional switch to occur in a duplicate of the ancestral oestrogen receptor (AncSR1), in order to produce the ancestral steroid receptor (AncSR2). The proteins have been further drifting apart ever since.

Just to remind you, estrogen is a steroid hormone. There are other steroids, such as androgens, that the authors claim were not part of the receptor capability of AncSR1

You're talking about the function of binding the hormone, not the DNA.

but they also acknowledge that the ancestor was "promiscuous" in function. That makes me suspect it may have had dual-functionality and didn't discriminate between steroids, although it was much more specific to estrogen than other steroids. Androgens exist in the zebrafish and, indeed, in most chordates.

I see that you are focusing on the hormone binding function of the steroid receptors, rather than their DNA binding capacity. It has two functions, one is the DNA binding capacity, the other is it's activation by binding the actual hormone. The hormone molecule binding is promiscous, the DNA binding capacity is not.

Let's try to get something clear here. These molecules are transcription factors, they have two distinct, molecule-binding functions. They bind DNA, and they bind hormones. I have been speaking about the DNA binding capacity of these molecules (that is the one the authors in their 2014 paper explicitly claim was NOT ancestrally promiscous).

It appears now you have been talking about the interaction with the hormone instead. I guess we have been talking past each other.

Funny how the need to make quantifiable statements about the size of the functional shift is now suddenly a requirement when the rhetoric is turned back against you.

Quantification helps when making radical claims, if you excuse the pun.

"You see a lot, doctor. But can you point that high-powered perception at yourself? What about it? Why don't you – why don't you look at yourself and write down what you see? Or maybe you're afraid to" - Clarice Starling

But they actually explain that the SR no longer interacts with the ERE (oestrogen response element, AGGTCA), and ER no longer interacts with SRE (steroid response element, AGAACA). They can no longer perform each other's functions. And the ancestral protein AncSR1 that gave rise to both classes (SR and ER) preferred ERE exclusively. So the function for interacting with SRE came after duplication and divergence of the two copies.

That is true. But how could the ancestral protein prefer ERE *exclusively* when, presumably, there were other steroid hormones produced in the organism that had this ancestral gene? Were there no males in the population?

Yes so you have in fact confused the DNA binding capability for the hormon-molecule binding.

My other point is that the paper only reconstructs the ligand-binding capability of all steroid receptors. It doesn't account for the fact that this class of transcription factor diverge greatly in ways that are not related with DNA binding affinity.

The work on the DNA binding and hormone binding are in different papers and are distinct functions. It actually makes perfect sense of the data. The duplications of the ancestral hormone receptor allowed distinct DNA binding capacities to evolve for specific versions of steroid hormones, rather than having a single hormonal regulator respond to lots of different related hormones.
"Nullius in verba" - Take nobody's word for it. https://en.wikipedia.org/wiki/Nullius_in_verba
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Re: Study find 100's of possible alternative evolutionary paths

#20  Postby Thomas Eshuis » Sep 19, 2017 8:23 pm

I see Wortfish has found yet another thread to wack his Dunning-Kruger off into.
"Respect for personal beliefs = "I am going to tell you all what I think of YOU, but don't dare retort and tell what you think of ME because...it's my personal belief". Hmm. A bully's charter and no mistake."
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