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From: John Harshman <john.harshman@gmail.com>
Newsgroups: talk.origins
Subject: Re: Red and yellow parrot feathers
Date: Sun, 3 Nov 2024 10:13:42 -0800
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On 11/3/24 9:49 AM, RonO wrote:
> On 11/3/2024 10:07 AM, John Harshman wrote:
>> On 11/3/24 6:13 AM, RonO wrote:
>>> https://www.science.org/content/article/why-are-parrots-so-colorful- 
>>> study-points-simple-chemical-tweak
>>>
>>> There is a link to the research article in this news piece, but it 
>>> may not be open access.  It is a pretty amazing molecular genetic 
>>> analysis coming out of an ecology and evolution group of 
>>> researchers.  They utilized genomic sequence, long read RNA Seq, 
>>> single cell RNA Seq, and regulatory sequences involved in gene 
>>> expression in feather cells.
>>>
>>> They identified the causative gene for turning red feathers yellow, 
>>> and the possible causative mutation that is segregating in one 
>>> species that is responsible for the recessive red feather 
>>> expression.  The difference in expression levels for the gene are not 
>>> that great, but there is a larger difference in single cell types.  
>>> The enzyme is expressed in all cells, but has higher expression in 
>>> the yellow feathers.  This increase in expression is enough to 
>>> convert enough red pigment to yellow to make yellow feathers.
>>>
>>> The only issue that I see in this paper is that they may not have the 
>>> causative mutation.  They mapped the causative gene because there 
>>> were 3 SNP (single nucleotide polymorphisms) found to be 
>>> significant.  They mapped to possibly a small region of the genome 
>>> flanking the ALDH3A2 gene, but two of the SNPs were on one contig and 
>>> 1 SNP was on another containing the gene.  This means that there are 
>>> issues with not having continuous sequence in this region.  It could 
>>> be repetitive sequence or issues with genome assembly.  What they 
>>> needed to do was long read genomic sequencing of the region to obtain 
>>> the continuous sequence in order to determine if they were dealing 
>>> with something like a retroviral insertion or some other assembly 
>>> issue.  The causative mutation may exist in the missing sequence 
>>> between the two contigs.
>>>
>>> In my own experience we have the recessive white allele at the C 
>>> locus in chickens.  This mutation turns out to be due to a retroviral 
>>> insertion in an intron of the Tyrosinase gene that causes 
>>> differential splicing in epidermal cells, but normal splicing in 
>>> other tissues. When you assemble a genome out of short reads using a 
>>> reference genome if the reference genome (in our case it was Red 
>>> Junglefowl that did not have recessive white) you get two contigs 
>>> cleanly separated from each other with the retroviral insertion 
>>> sequence missing.  These researchers may be having issues with 
>>> something similar.
>>
>> Do you know what causes the defective splicing in epidermal cells?
> 
> They do not know the cause.  For some reason the retroviral sequence 
> continues to be successfully spliced in certain tissues, but for some 
> cell types like epidermal cells there is a mess up and incorrect 
> splicing occurs so that a functional tyrosinase transcript is not 
> produced.  It is the reason why the early protein work on recessive 
> white found functional tyrosinase expressed in recessive white birds. 
> That is the reason that recessive white was a black eyed white. 
> Tyrosinase was still produced in the retina, but it wasn't produced in 
> the feathers or leg scutes.  Tyrosinase is produced in the dermis.  That 
> is why the normal junglefowl dermal pigmentation of the shank can be 
> express in white feathered breeds like the French Bresse breed of 
> chickens and recessive white Silkie that has pigmented dermal and 
> internal tissue pigmentation.  Silkies have black muscles, connective 
> tissue and bones.
> 
> The retroviral insertion affects splicing in a tissue specific manner.
> 
> https://www.ambresse.com/french-bresse-chicken.html#:~:text=Bresse%20growth%20rate%20outstrips%20the,higher%20prices%20in%20the%20marketplace.
> 
> Ron Okimoto
>>
> 
Perhaps the mutation introduces a binding site for some transcription 
factor or regulatory RNA that's expressed only in epidermal cells, and 
this happens to interfere with splicing?