Posted: Apr 17, 2019 3:26 am
by Wortfish
Rumraket wrote:
No, it clearly isn't. The segments being duplicated in stage C and F are the same, the Threonine-Alanine-Alanine tripeptide encoded by a 9-nucleotide repeat.


Please read the text and the quotes I provided:

B. "We discovered that the ancestral 9-nt element likely originated within a pair of conserved 27-nt GCA-rich duplicates that now flank each end of the repetitive (Thr-Ala-Ala)n cds in functional AFGPs."

C."We hypothesize that, upon the onset of selective pressure from cold polar marine conditions, duplications of a 9-nt ancestral element in the midst of the four GCA-rich duplicates occurred."

F."Subsequent intensification of environmental selection pressures likely drove the intragenic (Thr-Ala-Ala)n cds expansion forming large AFGP polyprotein genes (Fig. 4F) as well as additional whole gene duplications."

There are three stages of duplication claimed.

1. Duplication of a GCA-rich stretch of 27 nt ncDNA (Stage B).
2. Duplication of 9 nt elements within the duplicated 27 nt stretches (Stage C).
3. Final intragenic duplications of the TAA tri-codons (Stage F).


Then all the more reason not to think the authors are somehow stupid and would seriously postulate that selection somehow made duplications happen in a locus not being expressed.


Maybe they are stupid....or believe in some sort of Lamarckism where the environment induces mutations to happen.

There has to be some sort of limit to how stupid we should allow ourselves to think the authors are. You are familiar with the concepts of strawmanning and steelmanning? Rather than giving their words a deliberately hostile interpretation, try to be at least somewhat charitable and assume they can think.


We should never assume anything.

No, there is absolutely zero fucking reason to think they are claiming that, and only a braindead creationist tool with a pseudoscientific political agenda would deliberately ascribe to them this fatuous insinuation.


They make that very clear within the text.

What's a "completely chance" mutation and how would those be different from mutations happening even if a particular selection pressure is in operation? Natural selection doesn't make particular mutations happen. It instead acts to bias their rate of increase or decrease in frequency in the population when and if they occur, should those mutations have an effect on fitness.


The repeated bouts of microsatellite-like duplication of just the TAA codons (why not others?) are not just chance mutations but also extremely unlikely to the point of being wishful thinking.

No, it's a completely straightforward explanation of the pattern observed from comparative genetics of the sample of fish taxons being stuided. These are the types of patterns expected to exist if a protein coding gene evolved from non-coding DNA.


It isn't. The whole scenario presented is ridiculous. The worst part is the idea that the proto-sequence was transplanted to a new genomic region and the authors admit they have no idea how it happened:

We propose the possibility that the cis-promoter region was acquired in the most recent common ancestor of the AFGP-bearing clade through a stochastic translocation of the ancestral AFGP founder region to a new genomic site that happened to contain a TATA motif thereby conferring transcriptional capability. Although the specific mechanism of the translocation is currently unclear, cryptic transcriptional initiation sites and regulatory signals are deemed prevalent throughout genomes as increasing evidence suggests large portions of genomes become transcribed at some time.


What are you even talking about here?


Again. Read the paper:

The latent signal peptide (SP)-coding exons were fortuitous noncoding DNA sequence immediately upstream of the 9-nt element, which, when spliced, supplied a typical secretory signal......A functional AFGP consists of three exons and two introns. The first two small exons (E1 and E2) and the first two nts of the large third exon (E3) encode the SP, and the rest of E3 encodes a short propeptide and the long AFGP polyprotein.