the Blackest Ones: on exploring the significance of Cemani mutations

I went back and deleted my previous posts and I would ask all others to delete my post that is quoted. I will not debate the subject and will allow others to read the papers on the subject. Please disregard my post.

I have decided to leave this thread. I will start a thread on the subject.

Tim

I did start another thread and it is posted. I changed my mind and welcome all questions and comments. If comments are posted, please supply research quotes and the source that would support your position on the subject. I have supplied the research articles where I obtained the information. I can provide quotes from the manuscripts if an individual has a question about the information.

https://www.backyardchickens.com/t/...f-fibromelanosis-in-the-sikie-and-ayam-cemani
 
How can you tell she's not as dark *as the best* Cemani as a little chick --- or is that an old pic?
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I should have clarified. Yes, she hatched in November. This is a recent photo. It shows that her mouth is a dark grey with a light grey upper tongue surface. The photos I have seen of good quality Cemani show deep black mouths and black tongue.
 
I did start another thread and it is posted. I changed my mind and welcome all questions and comments. If comments are posted, please supply research quotes and the source that would support your position on the subject. I have supplied the research articles where I obtained the information. I can provide quotes from the manuscripts if an individual has a question about the information.

https://www.backyardchickens.com/t/...f-fibromelanosis-in-the-sikie-and-ayam-cemani
Thanks Tim
 
Hi my name is Craig and I live in Thailand. I have three different bloodlines for the black chickens. I really enjoy all the DNA conversation although I will say it's particularly helpful when I have insomnia. Please in no ways was that insulting,I love reading about it it's just so far over my head. Anyway I keep trying to get a darker and darker chicken. I still end up with a lot of the Mulberry. It is interesting that they farm them over here I found a guy that has over 2000 and sells them for allot per pound because the people love the meat.
Your summit I got from England.
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I edited this for additional clarification and information:

Some of the genetics discussion was indeed confusing. I'll make another attempt to clarify using the genetic symbols commonly used on this forum. For this discussion it is assumed that the chickens in any examples are id+/id+ and therefore don't have Inhibitor of Dermal mmelanin genes (Id) that prohibit fibromelanosis expression.

For my explanation:
FM = Fibromelanosis phenotype (chicken having black skin,tissues etc.)
Fm = Dominant fibromelanosis gene
Fm+ = Recessive wild type (not Fm).

Since each chicken has two sets of chromosomes and therefore two sets of genes, the possible combinations are:
fm+/fm+ = wild type (no FM)
fm+/Fm = FM (heterozygous)
Fm/Fm. = FM (homozygous)

Birds having two copies of Fm (homozygous) are darker than birds with one copy (heterozygous) birds. This is called incomplete dominance or semi-dominance. Externally they may look just as dark, but internally the heterozygous birds will show noticeably less dark tissues, often having areas of normal color mixed with the dark.

Most chicken color genes result from variations in genes (alleles), but fibromelanosis results region complex duplication called a Copy Number Variation (CNV). This complex duplication event also results greatly increased expression of some of the duplicated genes. Up to 10 times the expression of the EDN3 gene has been linked to fibromelanosis. The FM-locus comprises the duplicated region that results in fibrimelanosis. This Fm-locus containing multiple genes is inherited as a unit and does not segregate. The complicated nature of the CNV at the FM-locus is irrelevant for breeding purposes, we still use the same Fm, fm+ genetic symbols. They represent the presence or absence of the FM-locus.

This is how the genetic symbols relate to the FM-locus CNV using the same three possible combinations from above.

fm+/fm+ = wild type (no FM-locus CNV)
fm+/Fm = FM (heterozygous, one FM-locus CNV)
Fm/Fm. = FM (homozygous, two FM-locus CNV's)

In summary, knowing that FM is caused by a CNV is interesting, but doesn't really impact how we breed for the trait and doesn't make it anymore complicated.

The following is an excellent review of the current state of knowledge (as of 2013) and is put in terms that are easy to understand:

http://tru.uni-sz.bg/ascitech/3_2013/001-Fibromelanosis in domestic chickens.pdf

It also discusses the effects of interacting genes as well such as extended black and recessive white.
 
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