The Genetics of Fibromelanosis in the Sikie and Ayam Cemani

[nicalandia]

Cool birds, that skin seems to be the typical Fm outside cemanis.

I would so love to have a Cemani to test out the unknown modifiers idea. Two initial crosses- one with my Fm naked necks, one with fm+ naked necks.

The first to see if there's any clear immediate results in the F1, if not then intercross the F1.

The second to see if Cemani outcrossed to fm+ produces different Fm phenotype than non-Cemani Fm bred to fm+ then intercross and backcross- keeping this line totally separate from any other Fm birds. Do you agree if this line produces several birds clearly very dark that would be suggestive of Cemanis having modifiers?

Naked neck just because I love them but also it is a brutally honest signal of fibro quality. If the skin isn't that dark, it is way plain for all to see.

Thats a really good breeding Plan Kev...



now Back to Topic.. I get what Tim is saying, 4 Fibromelanotic genes because there is two mutation in one single gene..... yeah we get that..

but here is the Question that will settle this.....


Can any of those Mutants segregate separately?: and the Big Answer is NO they dont, So for all intents and purposes these two mutations can be regarded as a single Fm/? gene,



Edit.
From Source: http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002412

A characteristic feature of duplicated sequences is that they are prone to copy number variation due to unequal crossing-over. This is well illustrated by the dominant white locus in pigs that shows extensive haplotype diversity in breeds with the dominant white color based on the presence of 1–3 copies of a 450 kb duplication encompassing the entire KIT gene [30]. The FM rearrangement appears to be stable, unequal crossing-over is probably suppressed by the presence of an inverted copy of Duplication 2 located between the two copies of Duplication 1 (Figure 4).






so Again These two Mutants located on the same allele cant and wont seggregate separately..

 

[Kev]

Can any of those Mutants segregate separately?: and the Big Answer is NO they dont, So for all intents and purposes these two mutations can be regarded as a single Fm/? gene,

That's my thoughts if I understood this topic correctly. It being a duplication event is pretty much just way cool and new information about fibro but ultimately doesn't seem to require any changes in terminology as it still inherits as an simple autosomal. Similar to finding out c(recessive white) O gene are due to viral insertions, iirc.

It would be REAL nice to find out what are all the desired modifiers and their genetics, which still falls under this topic I think.

 

[nicalandia]

That's my thoughts if I understood this topic correctly. It being a duplication event is pretty much just way cool and new information about fibro but ultimately doesn't seem to require any changes in terminology as it still inherits as an simple autosomal. Similar to finding out c(recessive white) O gene are due to viral insertions, iirc.

It would be REAL nice to find out what are all the desired modifiers and their genetics, which still falls under this topic I think.

thats correct, you can carry on Treating the Fibromelanotic Trait as a simple Autosomal gene, needing id+ for fully expression, and on some cases Id can be inhibited partially by other genes, so even Fm/fm+ Id/id+ with other genes can express some traits, but on a smaller scale

 

[tadkerson]

 

[tadkerson]

 

[Kev]

If you know how linked genes work, it would be best symbolized using the same kind of genotype. Like spangling ( as in appenzellers) is mostly due to the expression of three linked genes. The genes are Db, Ml and Pg: all are found on one chromosome. I can not remember the distance between the different genes, I think it is about 10 cross over units, but they are not really close together like pea comb and the blue egg shell gene ( 4 units). When the linked genes are written as if they are linked the homozygous bird would be Db-Ml-Pg/Db-Ml-Pg.

The dark fibromelanotic bird would be written as Fm-Fm/Fm-Fm ( four EDN3 genes).

IMO that's considerably clearer than Fm/Fm/Fm/Fm. I hope you understand where my initial confusion came from. I was already familiar with Db-Ml-Pg and was going to suggest - for the duplication, using Db-Ml-Pg as the familiar model, instead of / in one of my replies but didn't want to jump too far ahead.

Quote:
Looking forward to it!

 

[tadkerson]

 

[urjtobreed]

The problem that I have with "Fm/Fm/Fm/Fm" is that it essentially means there is a homologous quadruplet and therefore 4 homologous chromosomes. A condition like this would only persist in hypothetical cells that divide into 4 instead of 2. This is clearly not the case here. Genes form homologous pairs that is why they are described in pairs and no more.

http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002412
A quote from this article:
"As these results have shown, this type of large-scale structural rearrangement of the genome has the capability to alter gene expression regulatory mechanisms at an extended range. This suggests that while this type of variation is inherited as a single locus it may have multiple downstream effects through perturbation of several different genetic pathways, possibly contributing to more subtle or complex phenotypes."

"Inhereted as a single locus" which means until someone gives evidence otherwise, it should be listed as such.

This article states:

"here we have adopted the currently recommended nomenclature system for the chicken where FM refers to the Fibromelanosis locus and *FM and *N refer to the dominant Fibromelanosis inducing allele and the recessive normally pigmented wild-type allele respectively. All birds expressing the FM phenotype are homozygous wild-type *N at the ID locus, or hemizygous in the case of females as ID is located on the Z chromosome."

They refer to a single locus and notate it as such. On this forum Fm and fm+ are often used, but they use *FM and *N.

Fm = *FM = dominant Fibromelanosis inducing allele
fm+ = *N = recessive normally pigmented wild-type allele.

Since it is inherited as a single locus, Fm-Fm/Fm-Fm would also be unnecessarily complicated and inappropriate.

There is more going on at the FM locus than just extra EDN3 genes. The EDN3 gene is also greatly upregulated (up to 10 times) due to other mechanisms inherent to the duplicated region. So it probably best to refer to it as the FM locus, since it is more complicated than just extra copies of EDN3.

 

[urjtobreed]

That was one of my thoughts- if the phenotypic difference is real, then possibly unknown modifiers are involved. An intimidating thought also-if the modifiers are unique/almost unique to cemanis then without crossing out to cemanis with modifier(s), it's possible no amount of breeding darkest to darkest in a project flock would achieve any even close to the jet black cemanis.

It'd have to be incredibly dark skinned silkie for me to consider as outcross. Haven't seen any.

Seems that way to me also. A few eb birds had dark skin, but cockerels lightening up as they matured was a constant issue. eWh is horrible for dark fibro expression, imagine that's no surprise to anybody though.

I'll open another can of worms here. We should also consider other mechanisms such as epigenetics (heritable changes in gene activity that are not caused by changes in the DNA sequence.

Some light reading:
http://www.sciencedaily.com/releases/2012/02/120229091844.htm
http://sweetwaterhrv.com/blog/heart-rate-variability/what-swedish-chickens-tell-us-about-dna/
http://www.epibeat.com/article-summaries/chicken-little-can-blame-epigenetics/984/

I bring this up because of something Resolution posted on "the Blackest Ones: on exploring the significance of Cemani mutations" thread.

Yes- I've noticed that a good number of the birds born of each hatch will be "Dragon Bone", that is black bones and white flesh and then there's all the morphs in between.

As for the survival issue, i do tend to believe that more chicks will hatch from embryos nurtured on egg yolks generated from animal protein enriched diets- and that perhaps soy bean meal negatively effects junglefowl reproductive health. With more chicks hatching from a selective breeding founder flock one will have more cemani morphs hatch.
Keeping them from developing problems along the way, reducing infectious disease and mortality of those chicks- I prefer a soy-free diet plan. I'll use ultrakibble chick supplement mixed into finch seed and unhulled sesame seed with generous amounts of fresh ground pepper and dried and/or fresh oregano/marjoram as the maintenance diet. If I do use chick starter it will comprise no more than 25% of the maintenance diet. In other words, I feed and maintain my black bone segregates like green junglefowl and I find that I produce many more cemani and other black bone morphs ( from other composite stocks bred to this mutation type) when I do so. It is my understanding that certain genes are turned on and off like a light switch and many of these will only become active when certain micro and macro nutrients are present in the diet from breeding pair on- it effects the mobility of sperm as well the nutrition quality of the egg yolk itself. These nutrients must be consistently available- within the maintenance diet throughout the birds life for optimal health-

I use UltraKibble supplement as a small amount goes a very long way and it is soy free, with animal protein and a wide range of nutrients required by many wild subtropical insectivorous bird species.

It may be possible that epigenetic changes contribute to the deepest black FM chickens. Resolution thought diet might help them hatch, but it also might help change gene activity to allow better FM expression. It may help explain why Cemani and Silkies in this country are not as black as they could be. What are Cemani in Indonesia fed? It could be that a good diet of bugs, greens and seeds may increase occurrence of the deepest black FM. I doubt there are many people in the USA who successfully free range their Silkies. There are probably few people who are willing to risk free ranging their expensive and rare Ayam Cemani. I free range my South American FM, but I do take my losses. I haven't avoided soy feeds, but I have had good hatches. Once I get to the point where I am not seeing increases in darkness, I may try a diet change. There may yet be hope in obtaining the deepest black FM in the USA. The genes may be hiding or they may just need awakening. The more that FM birds are bred with an eye for darkness, the greater the chance that the blackest genetic/epigenetic combination will come together.

 

[nicalandia]

I was already familiar with Db-Ml-Pg and was going to suggest - for the duplication, using Db-Ml-Pg as the familiar model, instead of / in one of my replies but didn't want to jump too far ahead.

You can treat its as if the two genes will segregate together most of the time. Is that what you mean by treat it as one gene?

Tim

Most of the Time? Thats Clearly an Overstatement, I mean Db-Ml-Pg are linked by like 10 cM or 10 m.u(1 map unit = 1 Centimorgan) where these genes clearly dont segregate independently and the P and O(P-O) genes are linked by even less than that(3 to 4 Map Units), now Fm-Fm linkage measuremets dont even use Map Units or Centimorgans, because that would be like measuring the distance between the tip of your arms in Miles instead of inches, so no, the Fm-Fm linkage is not measured in m.u or cM, they are meassured in bp(base pairs) and one centimorgan or map unit is about 1 million base pairs..


so again using the Db-Ml-Pg sample here is Absurd to say the least,

so For Simplicity Sake I will refrain from using Fm/Fm Fm/Fm(to indicate a homzygous fibromelanistic bird) or even Fm-Fm/Fm-Fm(to indicate a homozygous fibromelanistic bird) or Fm-Fm/Fm(a Heterozygous Fibromelanistic bird)... for Simplicity Sake I will only use Fm/Fm to describe a homozygous fibromelanistic bird or Fm/fm+ heterozygous fibromelanistic bird or fm+/fm+ non fibromelanistic bird,