The Genetics of Fibromelanosis in the Sikie and Ayam Cemani

[Kev]

FM also expresses extremely strong feelings and comments in humans. Attempt at humor, just have to have it sometimes.

I was frustrated for 20 years at lack of information and understanding and unfortunately, hostility from others- example, one well known breeder told me to completely drop my Fm projects after I made comments about the trait being so hard to understand and better breed for.... That almost broke my enthusiasm in those birds. I'm saying this because this topic seems to be constantly a tense one and it would be a shame to deflate any excitement over this trait or to make people who actually have and understand the information to be reluctant to share it.

So, thank you very much to both Tim and urjitobreed, both of you are deep breaths of fresh air and reignited enthusiasm in my own birds and Fm trait in general.


My question- if I understand right, Fm is caused by a duplication event of EDN3- yes or no? Is it limited to one duplication per region on each arm of chromosome or there can be up to four on the same region/arm?

 

[nicalandia]

My question- if I understand right, Fm is caused by a duplication event of EDN3- yes or no? Is it limited to one duplication per region on each arm of chromosome or there can be up to four on the same region/arm?

Correct, but since there is always two genes in a Pair, there will always be up to four on the same region, that is IF the Fibromelanotic bird is Homozygous for it..

 

[nicalandia]

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?

Actuallyt the Order of Mutation went like this..

e+ --- ER ---E ----eb( the first mutation was Birchen, then Extended black and there was Revertant Mutation of Extended black to eb brown)
e+-----eWh(dominant Wheaten)
e+ ----ey(Recessive wheaten)

For comparison, I'll post Morejohn's ey Jungle Fowl photo again:





A gene for yellowish-white down in the red junglefowl
Morejohn 1953
J Hered 44(2): 47-52
http://jhered.oxfordjournals.org/co...d.oxfordjournals.org/content/44/2/47.full.pdf

Note that these wheatens had dark undercolour (Morejohn, 1955).
Ref:
PLUMAGE COLOR ALLELISM IN THE RED JUNGLE FOWL (GALLUS GALLUS) AND RELATED DOMESTIC FORMS.
Morejohn, V.
Genetics. 1955 July; 40(4): 519–530.
http://www.genetics.org/cgi/reprint/40/4/519.pdf]http://www.genetics.org/cgi/reprint/40/4/519.pdf



The following table explains the MC1R (E locus) mutations in more detail:
Association of feather colour with const...(2003): Table 1
Quote:

Allele...71....92.....133....143....213....215
e+.......Met...Glu....Leu....Thr....Arg....His
ER.......–.....Lys.....–.......–.......–.......–
E........Thr...Lys.....–.......–......Cys.....-
eb.......Thr...Lys.....–.......–......Cys....Pro
ER-fay....–......–.....Gln.....–.......–......–
ewh/ey....–.....–.......–......Ala.....–.......–

 

[Kev]

Thanks.

So the point of contention here might be basically the idea a bird can have "three Fm genes"? according to your answer and I suppose urjitobreed's this is technically impossible? A bird can have three EDN3 but only the duplicated pair creates the Fm phenotype, and the third EDN3 on the other arm is essentially neutral and contributes nothing to the fibro phenotype?

I'm trying to keep it simple by asking one question at a time.... already have several in mind. Would it be better to list them or go question by question?

by the way I am trying to understand all positions(if there are differences). if there is any disagreement or differing answers to my question, please respond also.

 

[nicalandia]

Thanks.

So the point of contention here might be basically the idea a bird can have "three Fm genes"? according to your answer and I suppose urjitobreed's this is technically impossible? A bird can have three EDN3 but only the duplicated pair creates the Fm phenotype, and the third EDN3 on the other arm is essentially neutral and contributes nothing to the fibro phenotype?

I'm trying to keep it simple by asking one question at a time.... already have several in mind. Would it be better to list them or go question by question?

you got it right...

 

[Kev]

Okay I see it now.

Does it follow simple Mendelian genetics or not? with this question I am wondering if the extra EDN3 easily recombines or not.

 

[nicalandia]

Okay I see it now.

Does it follow simple Mendelian genetics or not? with this question I am wondering if the extra EDN3 easily recombines or not.

its an Autosomal gene, so yeah it does fallows Mendelian genetics, and recombination is extremely unlikely, the numbers are off the charts if you want to test it..

 

[tadkerson]

 

[urjtobreed]

Actuallyt the Order of Mutation went like this..

e+ --- ER ---E ----eb( the first mutation was Birchen, then Extended black and there was Revertant Mutation of Extended black to eb brown)
e+-----eWh(dominant Wheaten)
e+ ----ey(Recessive wheaten)
 

Thanks for the detailed explanation of the e-locus alleles. I'll read the links.

I was attempting to illustrate a point using a contrived incorrect statement about the e-locus as an analogy.

In other words, it would be incorrect to say that e+ IS the extended black gene (E). Likewise it would be incorrect to say fm+ is the fibromelanosis gene Fm.
It would also be incorrect to say that an e+/E chichen has two extended black genes when it actually has one wild type and one extended black. It is also incorrect to say that a chicken that is homozygous for fibromelanosis, has four fibromelanosis (Fm) genes.

Fibromelanosis is caused by a duplicated region of DNA containing extra copies of 5 genes. One of these extra genes (EDN3) is the likely cause of fibromelanosis. A homozygous FM chicken will have, on each chromosome 20, an original EDN3 and an extra EDN3 gene for a total of 4 EDN3 genes, but this does not equate to 4 Fm genes. The original two are wild type (fm+). The extra 1 or 2 copies with their extra gene expression cause FM and can therefore be called the Fm gene. So a single chicken can carry up to two Fm genes, not 4.

 

[Kev]

Okay thanks. Suspected that would be the answer but genes can play in very strange ways and just like to be completely sure.

Many sources make mention of Fm crosses as having light mouths and not as dark skin. Assuming dark mouth is an indicator of Fm/Fm, how come it seems to be a common experience(including mine) to be extremely hard to hit on dark mouthed chicks? If it is simple autosomal, there should be 25% or 1 out of 4 average.. yet it often feels like dark mouths comes up for one per 30 or 40 chicks.. a fair bit skewed.

also a common comment is fibro birds from projects or even 'purebred' silkies are not as solid, dark skinned like cemanis. Is this imagined due to exaggeration of Cemani traits or if the difference is real, then what exactly do the cemani have that are lacking in other fibro birds? I've never seen a pure cemani in person, so I don't know what to make of comments in regards to cemanis being "obviously darker than silkies". In many pictures they seem so DARK and I would not say mine are that jet black dark, even the dark mouthed ones.