Posted: 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.