the Blackest Ones: on exploring the significance of Cemani mutations
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Sigrid Van Dort has, Genetics of the Chicken Extremes, page 102 to 107 deals with both Fm, id"+", and the e-series the birds are based upon. Blackness (eumelanin) not just in the bone, but organs like skin, lungs, blood vessels, muscles, tendons, air sacs and nerves. She mentions no studies done yet on how genetics like lavender, barring/cuckoo, gold dilution, and mottled affect how black pigmented the birds are (dilutions and full stop of pigmentation so "white" no pigmented portions).
Which black and if there is a sheen depends on which s-series and hints abound that wild type autosomal red plays a part too. Melanotic and other extenders of black (aka recessive blacks) play a part also. Wheaten sucks if you want a self-black.
I have had communications with Dr. Roy Crawford (regarding my Booted Bantams having dark shanks), August 4, 2008 where he mentioned I was dealing with recessive white in conjunction with the Id locus...
Dr. Roy Crawford:
I have not read this thread front to back either, so cannot say if anyone has addressed the genetics you query about.
Good wishes in your pursuit of knowledge.
Doggone & Chicken UP!
Tara Lee Higgins
Higgins Rat Ranch Conservation Farm, Alberta, Canada
- Apr 27, 2011
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Melanism occurs in many animals including black breeds of chickens. This is different than the Fibromelanosis trait which results in hypermelanism of internal organs and is unique to chickens. Ayam Cemani has both traits.
Google "genetics of fibromelanosis". There is some fairly recent research which explains the genetic mechanism.
Here is the short of it:
All breeds tested with Fm trait have the same CNV (copy number variation) where a region of DNA containing 5 genes has been duplicated. The Fm trait is associated with the doubled expression of one of these genes: endothelin 3 (EDN3). This results in melanoblasts (pigment cell precursors) proliferating and migrating in an unusual route (ventrally) and invading internal tissues.
Fibromelanosis is incompletely dominant. Heterozygous individuals have reduced expression.
The ID gene blocks expression of Fm.
There are other unknown (recessive?) genetic factors that effect the degree of fibromelanosis, which makes breeding the blackest individuals difficult.
Fibromelanism has been linked to increased carnosine. However, I have not seen any research that explains what gene or genes results in the increased carnosine and if carnosine levels increase with greater Fm expression. It is conceivable that increased carnosine could result from one of the other 4 genes duplicated. I would be interested in seeing research on this.
Google "genetics of fibromelanosis". There is some fairly recent research which explains the genetic mechanism.
Here is the short of it:
All breeds tested with Fm trait have the same CNV (copy number variation) where a region of DNA containing 5 genes has been duplicated. The Fm trait is associated with the doubled expression of one of these genes: endothelin 3 (EDN3). This results in melanoblasts (pigment cell precursors) proliferating and migrating in an unusual route (ventrally) and invading internal tissues.
Fibromelanosis is incompletely dominant. Heterozygous individuals have reduced expression.
The ID gene blocks expression of Fm.
There are other unknown (recessive?) genetic factors that effect the degree of fibromelanosis, which makes breeding the blackest individuals difficult.
Fibromelanism has been linked to increased carnosine. However, I have not seen any research that explains what gene or genes results in the increased carnosine and if carnosine levels increase with greater Fm expression. It is conceivable that increased carnosine could result from one of the other 4 genes duplicated. I would be interested in seeing research on this.
Here's a group of 17 of my 'blackest ones' just hatched yesterday (single comb Fm LF ).
Not just blacks, there are blues and splashes also : )
Not just blacks, there are blues and splashes also : )
Great info. I wonder how it translates to mammals.
Was Cemani one of the breeds involved? Connective tissues are the target of the melanoblasts, right?
Quote: There are other unknown (recessive?) genetic factors that effect the degree of fibromelanosis, which makes breeding the blackest individuals difficult.
Knew it! The percentage of well-pigmented birds just is so unusually low- far too low to be a simple case of homozygous Fm and lacking Id and other better known genes that cause problems.
Tim- a frequent observation in regards to breeding fibromelanotics- it is significantly easier to get females with good Fm expression than mature males with good Fm expression. Many males lose varying degrees of expression as they grow- example gray skin at hatch, red/normal looking skin at full maturity- full maturity because some breeding age cockerels can have decent expression and lose a lot of it past one year of age. Testosterone is brought up as being the cause. Nothing solid as for genetics but perhaps that will give you a clue of some sort.
- Apr 27, 2011
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To further clarify, the e locus alleles in chickens that effect coat color are various mutations or alleles of the MC1R gene. Mutations to this same gene in other animals(including mammals and people) also cause similar coat/hair color variation. Mutations causing constant expression of MC1R cause black coat color and are dominant. Alleles for dysfunctional MC1R are recessive and cause lighter coat color. Mutations/alleles of MC1R effect abundance of melanins where they are normally found in feathers/fur/hair and a few other places.
The fibromelanosis trait causes melanin to be produced where it is not normally found in most animals.
Fibromelanosis results from a very different form of genetic variation than your typical coat color genes. It is caused by an unusual Copy Number Variation (CNV) that is entirely unique to only the chickens that carry it. This Fm causing CNV appeared in a single chicken or jungle fowl probably thousands of years ago and all Fm chickens are descended from that one bird. Through selective breeding, other genes that enhance the Fm trait have been accrued in breeds such as Silkie and Cemani.
Genes for black coat color (e locus/MC1R) are examples of known genes that enhance Fm expression in breeds such as Cemani. Other enhancing genes that make for the very blackest Fm chickens are more elusive. Perhaps multiple recessive genes that need to work concert. Perhaps there are also other unknown recessive genes that reduce expression of FM as well. Yellow skin is an example of a recessive gene that reduces Fm expression. This may explain how two of the very darkest birds when bred together can have many young that are not as dark.
FM makes dermal and connective tissues dark. Heterozygous FM individuals are not as dark and some connective tissues will not be melanized or will have black and white areas such as is often seen in the trachea. The most extreme expression may darken more than just connective tissue, for example the blood. Even though some people regard "black blood" a myth, there is evidence that it exists in rare individuals. Brian Reeder describes his personal experience with this in his book "An Introduction to Form and Feathering of The Domestic Fowl" Google his name and Fibromelansis Blood and you can read the relevant section. Indeed the best Cemani in Indonesia are said to have black blood, but this is also doubted by many. The darkened blood may be most evident when drawn rather than bled and exposed to oxygen.
The fibromelanosis trait causes melanin to be produced where it is not normally found in most animals.
Fibromelanosis results from a very different form of genetic variation than your typical coat color genes. It is caused by an unusual Copy Number Variation (CNV) that is entirely unique to only the chickens that carry it. This Fm causing CNV appeared in a single chicken or jungle fowl probably thousands of years ago and all Fm chickens are descended from that one bird. Through selective breeding, other genes that enhance the Fm trait have been accrued in breeds such as Silkie and Cemani.
Genes for black coat color (e locus/MC1R) are examples of known genes that enhance Fm expression in breeds such as Cemani. Other enhancing genes that make for the very blackest Fm chickens are more elusive. Perhaps multiple recessive genes that need to work concert. Perhaps there are also other unknown recessive genes that reduce expression of FM as well. Yellow skin is an example of a recessive gene that reduces Fm expression. This may explain how two of the very darkest birds when bred together can have many young that are not as dark.
FM makes dermal and connective tissues dark. Heterozygous FM individuals are not as dark and some connective tissues will not be melanized or will have black and white areas such as is often seen in the trachea. The most extreme expression may darken more than just connective tissue, for example the blood. Even though some people regard "black blood" a myth, there is evidence that it exists in rare individuals. Brian Reeder describes his personal experience with this in his book "An Introduction to Form and Feathering of The Domestic Fowl" Google his name and Fibromelansis Blood and you can read the relevant section. Indeed the best Cemani in Indonesia are said to have black blood, but this is also doubted by many. The darkened blood may be most evident when drawn rather than bled and exposed to oxygen.
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- Dec 5, 2012
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Here are some picsof my FM project. These are f4. This is my blackest roo so far he is only 6 months old so time will tell how well he holds it. Hens are easy to get black but roos are tricky.
Quote:
This is a fascinating discussion and I am learning a lot. I taught college Anatomy and Physiology for 25 years and blood is a connective tissue. The difference between blood and other connective tissue is blood has a liquid matrix, plasma, and other connective tissues have a solid matrix like bone or cartilage. In a normal living bird the only visible pigment in blood is hemoglobin which always red though the shade is effected by the level of oxygenation, oxygenated blood is bright red and deoxygenated is dark red. I suppose it would be possible for the blood to be dark all the time if the right genes were present in the bone marrow, where the blood is made, to add melanin during red blood cell production. .
This is a fascinating discussion and I am learning a lot. I taught college Anatomy and Physiology for 25 years and blood is a connective tissue. The difference between blood and other connective tissue is blood has a liquid matrix, plasma, and other connective tissues have a solid matrix like bone or cartilage. In a normal living bird the only visible pigment in blood is hemoglobin which always red though the shade is effected by the level of oxygenation, oxygenated blood is bright red and deoxygenated is dark red. I suppose it would be possible for the blood to be dark all the time if the right genes were present in the bone marrow, where the blood is made, to add melanin during red blood cell production. .
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