The Genetics of Fibromelanosis in the Sikie and Ayam Cemani

[tadkerson]

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.

 

[nicalandia]

Is it because of the gypsy face? or do they have other dermal/epi enchancers also? btw, what's the genetics for gypsy face?

Also thanks for rest of comment, I needed that reminder to myself of melanin expression, dermal/epidermal enchancers.

the Gypsy face is Trait(could be polygenic) that enhances the epidermis on these chickens, seems like Birchen does boost this abit more, but remember that Cemani birds may also have epidermal enhancers not just Dermal like Fm or id+, if you keep stacking them you will end up with the darkest one...


Also the mulberry face or Gypsy face can be found on other breeds, like the Sebright, the sebright genoe is ER/ER based and id+....











so if i had issues getting Full Black Faces on my Fibromelanotic stock i would start looking at gypsy faced birds to introduce that extra epidermal enhancer to make my birds as black as possible

Edit. Brown Red moder game Bantams show gypsy faces

 

[nicalandia]

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.

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,

 

[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.....–.......–

 

[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.

 

[KazJaps]

As you can imagine, nomenclature for mouse genetics is very advanced, needing to deal with quite complex scenarios:

STANDARDIZED NOMENCLATURE
http://www.informatics.jax.org/silver/chapters/3-4.shtml

Guidelines for Nomenclature of Genes, Genetic Markers, Alleles, and Mutations in Mouse and Rat​

​

http://www.informatics.jax.org/mgihome/nomen/gene.shtml#trdef

Quote:
There are several known coding elements within the first duplicated region including ATP5E (ATP synthase epsilon subunit), TUBB1 (tubulin, beta 1), SLMO2 (slowmo homolog 2) and EDN3 (endothelin 3).

NCBI Map viewer of EDN3 & the other genes within the duplicated region on Microchromosome 20:
http://www.ncbi.nlm.nih.gov/project...0]-r&QSTR=ATP5E&QUERY=uid(-2146617769)&zoom=1
----------------------------
Using the above mouse genetics nomenclature rules, the old Fm nomenclature could be expressed as EDN3Fm for the Fibromelanosis mutation, and EDN3+ for the wild-type. Ie once the structural gene is identified, you combine old allele symbols with the structural gene.
Therefore, you wouldn't do EDN3FmFm for the Fibromelanosis allele, as "Fm" defines all the sequence for the Fibromelanosis mutation. You don't use the old allele nomenclature to express structural gene duplications & other modifications. Also it wouldn't be accurate to leave out other structural genes within the duplicated region.

 

[farmerChef]

I have a Sumatra hen in with my Cemani crosses. The Cemani crosses are a gold birchen/brown red color. I also recently added 3 blue hens of mixed/unknown parentage, they hatched from olive eggs, day was supposedly an Ameraucana/Faverolles cross with black skin. Hatched 11/12 eggs, only 3/5 pullets had dark skin, no males. 2 have pea combs, so maybe they will lay green eggs too.
I also have a few Jersey giant hens, I lost their rooster last fall to a coon, but they will be moved out soon, I'm getting a blue boy next weekend. Going to hatch out a few of these to help with size, the Cemani crosses are on the small side. My 2 roosters are about 6 months old, I also have an older rooster, just over a year, who's comb is a mulberry color.

Year old rooster

 

[Pyxis]

Update: I have done that are now 12 weeks old, one is a cockeral too. Do far they're still completely black. Even the cockeral has absolutely no red beginning show in his comb or waddle.

I'm glad that they're staying black for you The point I was making in my last post though is that just being all black doesn't make a chicken an ayam cemani - otherwise svart honas wouldn't be a separate breed. So while you have created a crossbreed that has good fibro expression, they're not really 'AC look-a-likes', since they don't actually look like ACs in any way aside from being black.

 

[tadkerson]

 

[urjtobreed]

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.

******
The Fm gene was not duplicated, it was CREATED by the duplication!
******

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/