Wednesday, March 19, 2014

Visual "White" in Chicken Varieties

     Visual “White” in Chickens


Brian Reeder

It is so important to remember that all visually white areas on chickens are not the same thing. There are at least three major categories of “white”, plus a fourth group, a catchall for other genes that produce very specific white areas on the fowl.

Silver – in this context, silver is when pheomelanin (either/both sex-linked or autosomal) is diluted, suppressed or inhibited to turn red/gold/salmon pigment to lighter shades, and in the most extreme cases, to clean visual white. Amongst the genes that do this, the best known is sex-linked silver (S). However, S, on its own, is not enough to make a clean white visual phenotype. Along with sex-linked silver, there is also the inhibitor of autosomal pheomelanin (formerly referred to as ap+ in my writings, now referred to as Aph^I – Inhibitor of Autosomal pheomelanin). This gene inhibits the expression of autosomal pheomelanin and further helps to create the “clean white” that hobbyists desire on their silver varieties.

A clean "white" silver - this imported Ismer German Phoenix rooster showed the clean white Silver that all the imported Ismer Phoenix expressed.

A silver duckwing Phoenix hen showing expression of the Inhibitor of Autosomal Pheomelanin. Note the absence of any salmon tones in the breast. All of her plumage is cool tones with no warm tones, which is the hallmark of Inhibitor of Autosomal Pheomelanin expression.

In addition to these two major genes, dilution factors contribute to the cleanest white silver forms. The two recognized factors involved in this function are Dilute (Di) and cream (ig). Both are frequently extracted from clean “white” silver lines. Columbian (Co) and Dark brown (Db – ginger) both work with pheomelanin to extend it into eumelanic areas. Co has a strong repression effect on Aph and Mh and interacts most strongly with sex-linked pheomelanin. Db has a stronger interaction with Aph, but when Co and Db are together on the same bird, Co will tend to have a stronger effect, especially when S (sex-linked silver are present). Columbian can suppress the expression of Aph and Mh on the body of the bird when S is homozygous, without the presence of Aph^I. However, when Aph^I and Co are together with S, then the effect will be a very clean “white” silver Columbian or Columbian derivative (silver laced). All of these described forms of “white” are based on pheomelanic pigment inhibition/dilution and are thus referred to loosely as “silver” or “silvering factors”.

The next type of “white” is that which is made on eumelanin. In this type of white, eumelanic pigment is changed to visual white. There are several genes that do this and each likely has a different pathway to achieving its end. I group these together because the effect is achieved on eumelanic feathering. Some of these genes may have a mild dilution effect on pheomelanin, but it is generally slight and none of them will turn pheomelanic pigment to white. They only turn black feathers to white.

The first of these is dominant white (I). One dose of this gene will turn a black feather white with a few black specks. Two doses (homozygote) turns a black feather solid white, but it has little effect on pheomelanin and is used in the hobby to create red and white phenotypes such as “red pyle” (s+ e+ agouti e-allele with all black areas become white and the red areas remaining red), white laced red (a darker red version of golden laced in which the black areas have become white, but the red areas remain red) and Golden Neck (Mille fleur which is mottling on a Db s+ eb base with dominant white added so that you have a red bird with white mottling tips on the ends of feathers).

Dominant white heterozygote on an E/E self-black base. Notice the black flecks in the white plumage. This is a Cornish/Rock x Black Cochin F1.

The male in this picture shows dominant white with pheomelanin, demonstrating that dominant white removes eumelanin but does not remove pheomelanin.

The second of these is blue (Bl), which when heterozygous produces a grey feather from black feathers, but when homozygous becomes a smoky white with flecks of black and blue coloring in varying levels. Blue has little effect on pheomelanin, only diluting it slightly. Blue can interact with any other color/pattern form, just as dominant white does. So, with a homozygote for blue, (called splash in the hobby) one can make the white laced red, golden neck or red Pyle facsimile similar to those described above. However, this white will not be as clean as with dominant white, showing some cloudiness and flecks of black/blue, appearing much like the dominant white heterozygote.

The third gene in this group is dun (I^D), which is an allele of dominant white, occurring at the I–locus. The heterozygote turns all black feathers to a dull brown color, while the homozygote turns black to a near white with a shading of creamy brown and some flacks of dun as in the blue homozygote. Again, as in the two above examples, the homozygote can combine with any of the other color/patterns to make a facsimile of red pyle, white laced red or golden neck, amongst many others.

There is also a fourth gene, coming from Red Shoulder Yokohama, which behaves much the same as these three listed above. I tentatively dubbed it RSY^D (Red Shoulder Yokohamas Diluter) in 2003. In the homozygote, black areas become white, while in the heterozygote, the black areas range in a hodge-podge from black and blue to white in no discernible pattern or recognizable distribution. The most notable and commonly seen expression of this trait is white in the base of tail feathers in otherwise colored birds. I suspect this gene must be heavily modified as it has a wide range of expressions in regards to the amount of both white and/or bluish pigment that may be seen in heterozygotes. I suspect this trait is seen in many lines where white tail bases are a problem, as well as in many pit game lines where white tail bases are common.

In addition to Red Shouldered Yokohama, I have also extracted this gene from White Yokohama and White Sultans (though all White Yokohamas and White Sultans I have worked with do not have this factor). This factor has also apparently been extracted from some white Minohiki, which is no surprise, as the Red Shouldered Yokohama and White Yokohama (which also frequently carries this factor under the recessive white, just like the white Minohiki seems to) is a direct descendant of Japanese Minohiki.  Some have felt this is a type of mottling, but it is more likely that the white birds that carry this trait also carry mottling, as we see in the R. S. and White Yokohama and many other lines of white fowl, and that this gene is in fact a eumelanin diluter that creates “splashing” in the heterozygote state, but can be selected into a pure white expression that replaces eumelanin with visual white but not the pheomelanin, as we see in the Red Shouldered Yokohamas. Perhaps some lines of White Minohiki are just the RSD^Y factor homozygous and selected for a pure white expression in combination with Silver pheomelanin and the Inhibitor of Autosomal pheomelanin thus making the self-white phenotype. In either case, mottling could easily be masked in the homozygous state or carried in a recessive state as we see in many white lines of various breeds.

Here we see an American Longtail of Phoenix type that is expressing the RSY^D dilution factor in a heterozygous state on a red duckwing background with one dose of Dark brown (Db - ginger), also coming from the RSY. This is an F2 and is 1/4 Red Shoulder Yokohama (recessive white phoenix x RSY X red duckwing phoenix). Note how the areas that would typically be black are white with black splashed through it. This bird could easily be mistaken for pyle, which is based on dominant white on red duckwing.

Here we see a picture (albeit poor) of an American Longtail expressing the RSY^D factor in a heterozygous state on a golden duckwing background. This male shows the "blue, black and white" expression of eumelanin that can occur with this gene. Note that the breast is bluish and the tail and sickles are white and black.

To see more pictures from the web of Yokohama F1 crosses showing the expression of heterozygous RSY^D go to this thread on Backyard Chickens Message Board. In the first post, the third bird down, which is Blue Sumatra x White Yokohama, would be E/e+ at the e-allele and is probably S/s+ at the s-allele and melanized. Note how the RSY^D gene expresses as a pied or splash phenotype when heterozygous on this heavily melanized background with dilution of the pheomelanin. This bird could easily be mistaken for a splash from blue breeding, for an "over colored" exchequer-type mottling or as a Dominant white heterozygote. This is a beautiful bird and illustrates this effect perfectly. You can also see two more roosters showing the RSY^D heterozygous effect on the thread. The are the two birds in the fourth and fifth pictures on the first  post. Note that they are F1 backcrosses to the Yokohama, making them 1/4 Sumatra and 3/4 Yokohama. Note the similarity of dilution to the two males I have pictured above which are 1/4 Yokohama and 3/4 Phoenix. This form of dilution seems to be very persistent and can continue to express many generations after the initial outcross to Yokohama, finally expressing as nothing more than white in the base of the tail on an otherwise normal bird. A Google image search of 'Phoenix' or 'Yokohama' will turn up many pictures of birds showing this factor from crosses of Phoenix and other long tailed breeds Yokohama.

As a final point, for any of the genes in this category to make a solid white chicken, there must be no red/gold/salmon pheomelanin (i.e., no sex-linked or autosomal pheomelanin) expressed. Thus, a fully clean silver bird that is silver “white” and black can have these genes added to make a solid white bird or any of these genes can be layered on top of a solid black bird, even if red is present but covered with eumelanin to produce a solid white phenotype.

It is important to remember that such solid white birds are the product of both eumelanic and pheomelanic pathways and while they are visually simply white, they are using both the silver pathway and the eumelanic suppression pathway to get to the solid white visual phenotype. Many modification genes such as Columbian, mottling, Dark brown, Blue, Dun, Barring and/or eumelanic extenders (Ml, “rb”, etc.) may also be present to help create an under-coloring that is more easily whitened by these dominant eumelanic inhibitor genes. One well-known example of such a white phenotype is the White Leghorn.

The third group of white genes is those that remove both eumelanin and pheomelanin. These are the “recessive white” genes. Generally speaking, these are deletion genes or knockout genes. The first of these is recessive white ( c ) and is a well-known, and well-documented gene in both the hobby and research circles. This gene, when homozygous, removes all types of melanin, producing a solid white bird. The gene is recessive, so the heterozygote shows no effect.

A recessive white phoenix

The second is a less well-known recessive white. This form is not an allele of the better-known gene c. This gene removes all eumelanin and most pheomelanin, though a small bit of autosomal pheomelanin can show through, when such is present, giving a pale, ghostly peach/pink effect in the areas where it is expressed, notably, the male shoulder and female breast on e+ birds, thus to make a solid white phenotype with this gene, the autosomal pheomelanin must be suppressed. Sex-linked gold does not tend to show through this recessive white and is removed just as eumelanin is removed. Dr. Ronald Okimoto has typed this gene as mentioned in my book, An Introduction to Color Forms of the Domestic Fowl, and confirmed that it is a different gene from c.

In the phoenix lines in America, both types of recessive white that have been typed occur. It is therefore not unheard of to cross two white phoenix from different lines and get no white offspring, as the genes are not allelic. This second form of recessive white also occurs in some White Silkies and White Sultans. The above rooster is an F1 from a White Silkie x White Phoenix, both of which were the second type of recessive white. Note the slight expression of pheomelanin on the shoulder of this male - that is a diagnostic hallmark of this type of recessive white.

Here we see a group of young recessive white phoenix bred by Kim Mower that are the secondary type of recessive white which allows autosomal pheomelanin to express in the visual phenotype. You can see how strong this in the breasts of the hens, while there is only slight expression in the male. Interestingly, it is in an area where eumelanin is usually found 0 the legs and lower body. As these birds are Autosomal pheomelanic Silver duckwings with no ginger or Columbian additive factors, it is interesting that the removal of eumelanin by this form of recessive white that allows Aph expression, reveals Aph in a normally eumelanic area of the male. Birds of this type could easily be and often are mistaken for "silver pyle", but they are not, as this white is recessive when outcrossed, rather than dominant white, as in all "pyle" forms. Photo by Kim Mower.

A third type of this factor has appeared in Old English Game bantams, called pearl. It is a recessive gene which removes most of the eumelanin, leaving the hackles, saddle and shoulder of the male slightly tan/gray with the rest of the bird nearly white. I have never worked with this gene. This gene is occurring on solid black birds in the Pearl OEG and to date, I have not seen how it would express on any other base coloring. Further, it is not known if this gene has been tested against the second form of recessive white to determine if it is the same gene or an allele of the same locus. However, what is known is that on a black bird, the result of this gene is a near white phenotype.

Two genes, mottling and barring, produce the final category of “white” in chickens. These two genes have very different function. Mottling will produce a white tip to feathers on any background coloring, for the most part. There does seem to be some forms of eumelanic extenders that can suppress the expression of mottling, but generally, mottling will produce a white tip on any background coloring. Thus, we see black birds with white tip, red birds with a black bar and white tip or even red/gold/buff birds with a white tip and no black bar. There are two ways to achieve the later. 1. Add any eumelanic-removing factor (such as dominant white, homozygous blue or homozygous dun) to remove the black bar or, 2. Add pheomelanic extension factors (such as we see in a solid buff bird) to convert the black bar to pheomelanic pigment. In all instance though, the white tip shows through, as the gene seem to stop the production of any melanin (most any of them, expect, it seems, certain melanotic extenders such as recessive black factors) at the end of the feather. Finally, the level of mottling can be very variable and this may represent various modification genes interacting with one basic gene, or it could indicate that there are multiple alleles of the mottling gene, or it could be that there is more than one mottling genes at different gene loci. Exchequer may fall into any of these three categories.

Barring can produce white bars, but only on a black feather, so the white produced by barring is dependent upon the feather the gene is affecting. On a pheomelanic (red) feather, the barring factor does not produce white, but produces a paler gold/cream tone, so the white produced by barring is incumbent upon barring being on a black feather.

Finally, as an aside, the white crest of the white crested black Polish is something completely different from all of the other genes mentioned herein and seems to only effect the crest as the rest of the bird is black and in other instances this gene has been added to red Polish, making white crested red, showing that the white crest is restricted to the crest and does not effect either eumelanin or pheomelanins on the rest of the bird. It is likely that other genes that can produce some white in feathers exists and may be described in the future.

As you can see, there are many pathways to getting a visually “white” effect in the feathers of the chicken and all “white” is not at all genetically the same thing. First, there is the white that is pheomelanically derived and is called “silver”. Then there is the white that is eumelanically derived and is called “white”. Always remember that red becomes silver (both sex-linked and autosomal based upon their own dilution mutations) and black becomes white. While all of this is semantics, it is important in helping one to remember which type you are dealing with. The third type is the removal of all melanins and is total white, actually the near or total absence of all pigments in the feathers (not albinism!). The final white effect is through the patterning factors, mottling and barring. Mottling always produces the white tip (or more), while barring will produced black and white bars only when on a black feather. I refer to these as disruptors, as they disrupt the laying down of melanins. It is also important to remember that Pattern gene (Pg) does not produce white in and of itself. In those pattern gene based forms such as silver laced, silver spangled, silver penciled, etc, pattern gene (Pg) is only directing the pigments that are already there as to where they should go. Much like a conductor for an orchestra, pattern gene is directing where and when the various pigments should appear, not what pigments will occur. All silver patterned forms that show white areas with black areas are silver (group 1 of the visual “white” factors). If eumelanic reducing “white” genes are added, then such silver and black birds become either a blue or dun version or they become nearly or totally white, as the eumelanin is reduced partially or totally.

This issue of visual “white” in chicken feather pigmentation is a complex subject. It takes some time, effort and thought to really get a grasp on how this visually identical effect can in fact be so many different gene effects. The key to remembering what is what is to remember the different types of white that can occur. The most important distinction is between the pheomelanic form of “white” which is referred to as silver and the eumelanic-based forms of white. Though they can look the same, silver and “white” are not the same things, genetically, and are derived from very different pathways in the pigmentation process. Always bear in mind that there are four classes of white; 1. White derived through pheomelanin (silver), 2. White derived from eumelanin, 3. White derived through removing both eumelanin and pheomelanin (to lesser or greater extent) and 4. Those genes that produce white in specific areas only (mo, white crest) or through interaction with black feathers (barring).