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From: DB Cates <cates_db@hotmail.com>
Newsgroups: talk.origins
Subject: Re: Red and yellow parrot feathers
Date: Sun, 3 Nov 2024 19:48:56 -0600
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On 2024-11-03 3:38 p.m., RonO wrote:
> On 11/3/2024 12:13 PM, John Harshman wrote:
>> 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?
>>
> 
> My take is that it will eventually be figured out because it is an 
> unusually regulated mutation.  Something is interferring in epidermal 
> cells, and it should be some type of tissue specific regulation.  The 
> crazy thing is that it might have something to do with temperature 
> sensitvity like a reverse of siamese cats tyrosinase (active enzyme is 
> only produced at below body temperature in affected cats).  In this case 
> recessive white chicks can hatch with black down for some chicks, so the 
> correct splicing can occur when the skin is 37 degrees C, but not for 
> all cases.  Most of the time the down lacks black pigment.  The black 
> downed chicks feather out white.  The same feather folicles that 
> produced black down before hatch produce white chick, juvenile and adult 
> feathers.
> 
> Ron Okimoto
> 
Thanks for things like this. Something to pique the interest of a high 
ignorance of the subject individual like me and a reminder that life is 
a very weird and convoluted chemistry hack.

-- 
--
Don Cates ("he's a cunning rascal" PN)