Posted: Apr 17, 2019 11:10 am
by Rumraket
Wortfish wrote:
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).

None of which contradicts what I said.

Wortfish wrote:
Rumraket wrote: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.

Which there is zero reason to think. In fact the authors state the opposite:
Proto-ORF Model of de Novo Evolution of Gadid AFGP.
The deduced evolutionary process of the gadid AFGP gene from non-sense DNA adds valuable insights into how adaptive functional genes could arise “from scratch.” The birth of de novo genes involves two fundamental events: the formation of an ORF and the acquisition of regulatory signals for transcription. In principle, these events could occur in either order. This prompted two major competing models: the protogene versus the proto-ORF model (3, 17, 29⇓–31). The occurrence of a protogene is generally easier to detect as the de novo gene has a noncoding ortholog with demonstrable transcripts in the out-group species. Thus, the model has found ample support in studies that showed transcription preceded the emergence of an ORF (6, 17, 30, 32). The proto-ORF model states that an ORF was present before regulatory signals for expression were acquired. The existence of proto-ORFs is challenging to prove as they likely accumulate mutations that would interrupt the ORF before they could become transcribed for selection to act upon (3, 29, 30, 33).

This shows the authors understand that there could not have been selection operating on the gene before it acquired a transcriptional promoter. So there's no other way to make senes of their words than selection driving the expansion of the Thr-Ala-Ala tripeptide in stage F.

Wortfish wrote:
Rumraket wrote: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.

Then stop assuming the authors are stupid, or lamarckians, when there's zero evidence to support it, and only evidence against it.
Wortfish wrote:
Rumraket wrote: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.

That there's zero reason to think they're claiming it? I agree.

Wortfish wrote:
Rumraket wrote: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.

Microsatellite duplications of repetitive DNA is very common. The longer a repetitive sequence is, the more likely it is you get unequal crossover during homologous recombination because you will get stretches of homologus alignment even if the sequences aren't perfectly aligned.

Microsatellite DNA mutations that increase or decrease the number of repeats are so common they are used in DNA profiling and paternity testing, and in forensics because they are so likely to mutate and change in number that they exhibit significant change even over single generations, from one person to it's offspring.

Microsatellite repeat expansions are common drivers of certain neurodegenerative diseases such as Alzheimer's and certain types of frontotemporal dementia caused by CAG repeat expansions (so-called polyglutamine tracts). The more of them you have, the more likely they are to expand further(again, because the longer the repetitive sequence becomes, the more likely it will be misaligned during crossover), causing further and earlier lifetime cognitive decline.

There's nothing unusual or wishful thinking about these duplications. On the contrary, absense of such duplications in a repetitive area of the genome is the unlikely option.

Wortfish wrote:
Rumraket wrote: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:

Transposition of gene duplicates is an observed fact. It happened in the LTEE when the citrate transporter gene was duplicated into a different area of the E coli genome under control of a completely different promoter. So it's "so miraculously unlikely" that scientists literally watched it happen in a laboratory experiment. That's one of the mutations responsible for the cit+ ability under aerobic conditions, because the previous promoter was inhibited by the presence of oxygen.

There are a myriads of ways known that can facilitate this, of which low levels noisy transcription and subsequent reverse transcription is just one.

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.

Heh, yes. As I were just suggesting.

Wortfish wrote: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.

Yeah what's the problem? Introns are defined by the existence of splice site sequences. These recognition sequences are quite short and can exist many places in noncoding DNA entirely by accident. A whole host of similar and not completely identical sequences can be recognized and spliced.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1522026/


PMC1522026_1471-2105-7-263-4.png


PMC1522026_1471-2105-7-263-4.png (83.55 KiB) Viewed 1059 times




Logos of donor and acceptor splice sites. A graphic representation of aligned donor and acceptor splice sites. The relative heights of letters correspond to frequencies of bases at each position. The degree of sequence conservation is reflected in the total height of a stack of letters, measured in bits of information.