The Genetics of Fibromelanosis in the Sikie and Ayam Cemani

I was hoping my input into this thread would have some educational value but it appears that my input is not needed. The remainder of my postings on this thread will also be deleted because it does not really explain the inheritance of fibromelanosis; it is a debate that serves to nullify the original intent of the string.

Thanks for starting this thread Tim!!

tadkerson said:

Genetics 101


An example of a cross.

Dark black bone male carries 4 Fm and Two dermal melanin genes

Wheaten marans female carries 2 Fm and one dermal melanin inhibitor

dark black bone male x wheaten marans =

F1 chicks each with three Fm genes but the male and female offspring will not be the same even if they carry three Fm genes. The dermal melanin and dermal melanin inhibitor genes play an important role in pigmentation.

The F1 males inherited one dermal melanin inhibitor gene from the mother and will have light skin. The F1 males can pass on the dermal melanin inhibitor gene to some of his daughters and some of his sons; the daughters and sons can produce some light skin offspring even if a daughter or son is back crossed with a very dark mate.

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Tim you are describing a Basic SexLinked Cross


The Male´s Genome would be E/E(Extended Black, but they could also be ER/ER Birchen) Fm1/Fm1(Fibromelanotic gene1) and Fm2/Fm2(Fibromelanotic gene2) id+/d+(wildtype sexlinked dermal melanin gene, need it for full expression of Fibromelanotic)

The Female´s Genome would be eWh/eWh(Wheaten) fm1+/fm1+(Marans dont carry Fm on any form) fm2+/fm2+ Id/-(Hemizygous Dominant Sexlinked Dermal Inhibitor)


Now this cross will produce 100% Sexlinked chicks,

The Females will inherit the id+/- Z-Linked from their father and since these F1 females would also be E/eWh Fm1/fm1+ and Fm2/fm2+ they would be Nearly as black as their Father, they would also be Sexable at hatch, the F1 females will ALL have black skin at hatch

the Males of this cross will inherit the Z-linked Id(dermal inhibitor sexlinked) gene from mother and one Z-linked id+ gene from father so that would make them Id/id+ it seems like Id is Nearly completely Dominant on this scenario, so the F1 males all of them will have white/yellow Skin at hatch making them sexable too(different from F1 sisters)..


My limited experience with Fibromelanotic birds was when I was trying to produce Cemani look alike with native fibromelanotic stock from Nicaragua and White Leghorns, and since I was only able to get Spent battery white Leghorn hens I had to cross a fibromelanotic male to the leghorns, producing 100% Sexable chicks at hatch, that was like 8 years ago,

I applaud all of your efforts to make this easily understandable, even though it can be quite confusing. I hope my comments will help you make your guide even clearer.

Before fibromelanosis was known to be caused by a copy number variation (CNV), it was conventionally named in the same way as variation in genes (alleles) are described. The symbol Fm is used to describe the presence of the semi-dominant gene and fm+ as the recessive wild type. Using this convention, a single bird can only have up to 2 dominant Fm genes. Mixing the concepts of CNV's and alleles is where this gets confusing. Even though only the number of copies of the genes vary, fm+ must be used for the original copies and Fm must be used for any additional copies, because that is how the fibromelanosis trait is expressed.

fm+/fm+ has just the original DNA ("section 1" in your example) on both sets of chomosomes.

FM/fm+ has the original "section 1" on both chromosomes plus an additional "section 1" on just one chromosome.

Fm/Fm has the original "section 1" on both chromosomes plus an additional "section 1" on both chromosome.

These 3 examples are the only possible combinations.

I believe that if you use the symbol fm+ for wild type in your guide it will greatly clarify it and enable you to not incorrectly represent that a single bird can have 4 dominant "Fm" genes.

Before this particular duplication (I'll call it "FM-CNV") ever existed there was no fibromelanosis or Fm gene.
Also there is no Fm gene in chickens without the FM-CNV.

No FM-CNV = wild type.

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The Fm gene was not duplicated, it was CREATED by the duplication!
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The normal 2 copies of EDN3 = wild type or fm+. 2 EDN3's are normal and wild type.

One extra EDN3 gene (1x FM-CNV) = Fm/fm+.
Two extra EDN3 genes (2x FM-CNV's) = Fm/Fm
No extra EDN3 genes (no FM-CNV) = fm+/fm+

The original EDN3 genes are not Fm genes. It is confusing, because they are all identical EDN3 genes, but it is only the extra gene products of the extra EDN3 genes that make fibromelanosis. The abnormal levels of EDN3 gene products are what promotes the abnormal pigmentation.

The following researchers concluded semi-dominance. Their pictures of reduced FM in heterozygous individuals matches my own experience including the mottled trachea.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3276631/

I am sorry you are frustrated. So am I. You said you were willing to discuss comments, so I offered them. I would have left your post completely alone, if you had simplified the subject while being accurate. In my opinion you complicated it with incorrect statements. Simplifying and using non-technical terms is great, but somebody will try and correct you if you make wrong statements. Making wrong statements is not helpful or simple.

Saying that the original EDN3 gene, at the original locus, is the Fm gene is wrong. It is wild type. One could call, the duplicated EDN3 gene at the new locus, Fm, but not the original.

It is like incorrectly saying: "e+ (wild type) is the extended black gene". Extended black (E) is a mutation of the gene at that e-locus. You would never say that "a wild type chicken has the extended black gene". Eliminating mention of e+ would indeed be a simplification, but an incorrect and unhelpful simplification. So why would you insist that a wild-type bird has the Fm gene?

I think what you are trying to do is great. I believe your guide will be helpful if it done correctly. I hope you are not discouraged. If you are truly interested in helping people understand, you would be interested in hearing and considering why I think some of your descriptions are the opposite of helpful. This is a public forum, if you want to make uncontested statements, put it on your own website.

I am sorry to muddy up your thread, but I am trying to be helpful to you and the people reading it. I'll be willing to delete my posts to clean up your thread, when your guide is fixed and I think they are no longer necessary.

I think both versions are fabulous so that everyone is able to learn the basic concepts and THEN move on to expanding the ideas once they have the basics under their belt.

Just having you guys post this means that we can learn, then maybe go off and read some papers and then come back and read the posts again. This info is impossible to come by in a condensed and readable form so all imputs are invaluable to those of us that know less than you.


Please post ALL you know on the subject. I have a gazillion questions..

eg.:
What are the genes involved actually expressing? presumably tryosinase to convert the Tyrosine or one of its down stream products to (eventually) melanin.
BUT what are the modifiers doing? are they receptors? are they blocking or facilitating some some biochemical pathway?
How is it that so much melanin in the tissues is not toxic to the tissues?
Melanin (at least some forms) is an antioxidant, but when denatured becomes a nasty oxidative substance.
Do the FM birds have shorter life spans or fertility?
Is the brain tissue also black?

If anyone knows any of this or any info PLEASE post so that all this can be found in one place.

This info is impossible to come by in a condensed and readable form so all inputs are invaluable to those of us that know less than you.

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And very much appreciated : )