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).

Wednesday, February 26, 2014

The Genetic Factors of Silver Phenotypes


Brian Reeder

First published December 2011 in Exhibition Poultry E-Zine

     What does it take to make a red variety into a silver variety? Most people will simply answer that the sex-linked pheomelanic gene Silver (S) is all it takes, but this is not the case. In fact, getting to a good, clean “white” silver phenotype is much more complicated than simply adding the Silver sex-linked pheomelanic allele to the s-locus. For the last twenty years, I have been working toward understanding the differences in silver and red phenotypes. In that time, I have made hundreds of test matings and raised literally thousands of birds, and with each of those matings, I have gathered data on the segregations of the silver and red phenotypes, in addition to any other data I may have been gathering. By working with such large numbers, I have been able to, first, form a series of hypothesis about the various factors involved in these phenotypes, and second, to test those hypotheses repeatedly and within many different genetic populations, polishing them as more data emerged. Through all that work I have come to a good working understanding of the various heritable factors (genes) involved in these phenotypes.

     In the April 2011 issue of Exhibition Poultry, I wrote an article titled Pigmentation of the Red Jungle Fowl. That article is the precursor to this article, and I would recommend that anyone seriously interested in this article should download the April 2011 issue of this magazine from the website and read over that article as a companion to this one. I will be using my original artwork from that article to illustrate the progression of genes that make the final, fully clean white silver phenotype. I will also be using the MC1R gene, that we call duckwing in the hobby and notate as the e-locus allele e+, as the main base to illustrate this progression from red to silver phenotypes. However, this information does not only apply to the e-allele e+. The exact same heritable factors I will be discussing herein on e+ are used on all the e-alleles to go from the red versions to the clean white silver versions. In time, I will discuss the interactions of these factors on all of the e-alleles, but for the interest of brevity in this article, I will only be using e+ in the examples. The important thing to keep in mind when applying this information to e-alleles other than e+ is that each e-allele distributes the pigments (eumelanin, Sex-linked pheomelanin and Autosomal pheomelanin) in its own unique manner, and more so in the females than the males.

     To begin, let us have a quick reminder of the pigment makeup of the red duckwing, as seen in the red jungle fowl and varieties of domestic fowl similar to it, which I call red duckwing and is commonly referred to in the hobby as black breasted red (image 1). This variety includes eumelanin, the red form of sex-linked pheomelanin (s+), autosomal pheomelanin (Aph), mahogany (Mh) and usually includes dilute (Di). However, the presence or absence of Mh and Di do not change the phenotype from red and these are simply additive genes that create different shades of red/orange.

Image 1 - the typical red duckwing pair which is the color pattern of the red jungle fowl

     In both sexes, Autosomal pheomelanin is the base pigment that lies underneath the other pigments. In the male red duckwing, the body is eumelanin, while the hackle, saddle and main wing triangle are predominantly sex-linked pheomelanin while the shoulder and top of the head show the greatest saturation of Autosomal pheomelanin and also Mahogany (as Mh requires the presence of Aph to express visually – Aph serving as the platform upon which Mh saturates). In the female red duckwing, the breast expresses Autosomal pheomelanin while the back, shoulder, wing, cushion, tail secondaries and sides of the body are a complicated layering/blending of Autosomal pheomelanin, sex-linked pheomelanin and eumelanin. The hackle is mainly sex-linked pheomelanin with a eumelanic stripe in each feather, while Autosomal pheomelanin is predominant at the top of the head and around the outer edge of the hackles. For more on this red phenotype, refer back to my April 2011 Exhibition Poultry article mentioned above.

     So now, if we simply add the sex-linked silver gene to the red duckwing, what does the phenotype become? To begin with, it does not become an exhibition silver duckwing. The female can only have one dose of this z-chromosome, sex-linked gene, while the male can have one or two doses. (We will only be discussing the homozygous silver males (S/S) here in all of these examples. The heterozygote males (S/s+) are visually very confusing and can appear similar to any of these phenotypes we will be discussing. Since they are not true-breeding phenotypes, they are irrelevant to this discussion). In the male, the addition of homozygous Silver (S/S) to the red duckwing creates a phenotype that would be referred to as “gold” in the hobby (image 2). The homozygous Silver changes the hackle, saddle and wing triangle to a yellow/gold color, as Aph is still present and underlies all the sex-linked pheomelanic areas, so that when the Silver gene removes the sex-linked pheomelanin the Autosomal pheomelanin is still there and is visible as the golden hue. If mahogany is present, it is also not affected by the sex-linked silver gene and will still be seen on all of the usual areas of expression and will make the tone of the gold in the sex-linked pheomelanic areas somewhat darker than if mahogany is not present. 

Image 2 - the basic red duckwing combination when the s-allele s+ is replaced with S, but no other modifications are made

In the case where mahogany is not present, all the areas where mahogany is usually seen will express as an orange/peach/golden tone that is several shades darker than the hackle/saddle shades. In the female, when we add S to replace s+, the hackle is changed to a creamy white shade while the rest of the bird remains very similar to the red duckwing hen. The major factor that will be visually different is that the back will be a cooler shade with a gray/gold tone rather than the more warm brown of the red duckwing hen. This hen is the “golden”/”golden duckwing” standard type hen as found in the standard description for that variety, such as in Modern Game. If the hen is expressing mahogany, it will be visible on the head, around the hackle and will darken the back and breast to a more reddish tone. This phenotype, in both males and females can easily be confused with both Diluted and Cream forms of red duckwing.

     So how then do we get to a clean silver duckwing phenotype? The key is to remove (or inhibit) the Autosomal pheomelanin. In my earliest research with Autosomal pheomelanin, I believed that we had a simple pair of alleles at one locus and I called those Ap and ap+ (the + being applied to the absence of Autosomal pheomelanin as I felt it also derives from a wild source – the gray jungle fowl, just as the yellow skin gene in domestic fowl has been shown to derive). However, subsequent research and test matings have shown that these two factors are not alleles of one locus. They are in fact two separate factors and are non-allelic. As I described in the April 2011 Exhibition Poultry article, I now use the abbreviation Aph for Autosomal pheomelanin. In addition, since the inhibitor of Autosomal pheomelanin is not an allele of Aph, I am now using the abbreviation Aph^I (Inhibitor of Autosomal Pheomelanin).

     So once we have replaced red (s+) with Silver (S) we find that we still do not have a true silver duckwing, so we add Aph^I to inhibit the Autosomal pheomelanin. With only one dose of Aph^I (image 3), we see only partial inhibition of Autosomal pheomelanin. The heterozygotes for Aph^I will be lighter than the pair described above, showing a creamy, yellow/white tone in the sex-linked pheomelanic areas. In the female, the breast will show some spottiness, often with each breast feather showing a very pale pheomelanic edge. One of the most interesting aspects of Aph^I is that since mahogany only expresses on Aph, when Aph^I is present, the expression of mahogany is also suppressed. Thus, in cases where there is one dose of Aph^I, even when there is homozygosity for mahogany, very little expression of mahogany will be seen in the phenotype. The most prominent expression of mahogany will be on the male shoulder/back and the female shoulder/back and breast.  

Image 3 - When there is heterozygosity for the inhibitor of autosomal pheomelamnin (Aph^I), the phenotype is lighter and mahogany has far less expression

However, when even one dose of Aph^I is present, the mahogany expression will never be solid, and will only be spotty showing several shades of orange/red/mahogany. Two doses of Aph^I will nearly completely suppress the mahogany, so that only a tiny amount is seen at the edge of the shoulder/back area of the male. (I suspect there may be at least two alleles of Aph^I, as there is some evidence that a second form allows expression of Aph and mahogany in females, but suppresses it in males. Certain lines of gray Dorking in England, for instance, seem to attest to this but I have not had any examples to test mate or observe to date. It seems this alternate allele of Aph^I allows for clean silver males and Aph expressing females. In this regard, this allele of the inhibitor seems to show sex-expression of autosomal pheomelanin, with female expression and male inhibition. I hope to comment on this seemingly alternate allele after I have studied and test-mated it further in a future article.)

     In instances where there is one dose of Aph^I, but no mahogany, we see the phenotype in the male that is called “golden”/”golden duckwing”, as in the standard description of the Modern Game variety. The standard description calls for this phenotype of male, but the female called for in that standard form is the non-mahogany form described above in the previous section. The male of this type has a yellow/cream hackle, saddle and wing triangle while the shoulder is a darker yellow-gold to pale orange-yellow. Ironically, it is the female of this type, a heterozygote, that is the standard ‘silver”/”silver duckwing” hen. She has a gray back with a slight cream tint (silver pheomelanin with black/eumelanic stippling of any size appears visually gray and layered over a small amount of Aph, there is a creamy effect), the hackle pheomelanin is white/near white and the breast is salmon, generally with a paler lace of cream pheomelanin at the edge of the breast feathers.

     The true, fully silver phenotype (image 4) is very rare, because the female is not a recognized variety of any kind and most people, upon seeing one for the first time, think she is some type of Columbian or Ginger heterozygote. These hens are rather startling if you have never seen one, as the breast is extremely pale, almost completely silver, with almost no salmon expression at all. She also has no warm tones at all in any area of her feathering. When these hens do turn up in most breeding programs, they tend to be culled out as they are generally undescribed and non-standard. 

Image 4 - the fully clean, "white" silver phenotype seen with full, homozygous inhibition of Autosomal pheomelanin

Of course, the few people in the know make full use of these hens and they produce the cleanest white, Silver males. Silver/Silver duckwing has always been a double-mated variety, however, few breeders have ever known that and cull out the proper females. This knowledge has long been a carefully guarded “trade secret”. The ironic thing is that breeders of Silver varieties are constantly complaining about “brassy” silver males, yet they routinely cull out the females that could produce the proper males. The true Silver phenotype is homozygous for Aph^I. The female is as described above and the male is simply a black and stark white combination, with all the pheomelanic areas, both Autosomal and sex-linked, reduced to white. In many instances, these males show a small amount of white at the upper breast and may show a few spots of white in the lower breast.

     In addition to the presence of S, Aph^I and mh+, most silver varieties I have test mated also carry dilute (Di) and/or cream (ig). I am not sure that either of these genes is actually necessary to get clean silver, but they certainly don’t hurt, either. Any diluter gene is only going to help remove brassiness from the silver areas. The presence of these diluters should come as no surprise. These varieties were developed long before genetic knowledge, so it only makes sense from a visual perspective that those breeders would have used any pale pheomelanic birds in their efforts to breed silver, just as any diluters and whitening genes were used in the development of solid white birds (which are known to often carry many dilution factors in addition to the major whitening gene; recessive (c) or dominant (I)).

     As you can see from this discussion, the Silver varieties are much more complicated than the simple addition of the sex-linked pheomelanic allele Silver (S) to a given red variety. This discussion applies to any silver form of any variety. That means that all silver varieties, if they are clean, true white-silver combine homozygous Silver, homozygous Inhibitor of Autosomal pheomelanin and homozygosity for the absence of mahogany and may often also incorporate Dilute and/or cream, in addition to the other genes required to make the given variety. For those comfortable with using gene abbreviations, the genes of silver are S/S (S/~ in females), Aph^I/Aph^I, mh+/mh+ and often Di/- and/or ig/ig.

The Expression of Autosomal Pheomelanin (Aph) and the Inhibitor of Autosomal Pheomelanin (Aph^I) when in the presence of Columbian (Co) and Dark Brown (Db – aka ‘Ginger’)

The Expression of Autosomal Pheomelanin (Aph) and the Inhibitor of Autosomal Pheomelanin (Aph^I) when in the presence of Columbian (Co) and Dark Brown (Db – aka ‘Ginger’)

Part 3 – Originally Published November 2012 in Exhibition Poultry E-Zine


Brian Reeder

In my last two articles I have discussed Autosomal Pheomelanin (Aph) and the Inhibitor of Autosomal Pheomelanin (Aph^I) and their main interaction genes (September 2012) as well as the effects of both factors on the five most commonly encountered alleles of the e-locus (October 2012). This month, we will look at the last major (known) genes that interact with Aph and Aph^I: Columbian (Co) and Dark Brown (Db – aka ‘Ginger’).

Both of these factors are commonly called ‘eumelanin restrictors’ in the published literature on poultry genetics. I tend to refer to them as ‘pheomelanic extenders’, which is for all intents and purposes the same thing. The intent of either term being that these factors restrict eumelanin (black pigment) in the breast of the male, or extend pheomelanin (red/gold/silver pigment) into the breast of the male. However, restriction/extension is not the only function of these two genes.

Another major function of these genes is that they interact with Pattern gene (Pg) and Melanotic (Ml) to create the most widely known and beautiful patterns of exhibition and landrace poultry; namely autosomal barring, spangling (the real one, not mottling) and lacing. Dark brown (Db) is in fact linked to Pg and Ml as part of a fairly tight linkage group. Co is not linked with this group, yet works with these genes to create a unique expression of patterning (lacing).

When Db is found with only Pg, we see the pattern known as autosomal barring, as seen in campiness and “penciled” Hamburg. When Db and Pg are also found with Ml, we see spangling as in the Spangled Hamburgs. When Co is found with Pg, there is very little pattern, as without Ml, Co overpowers and washes out Pg. When Ml is then added, we see lacing. The two e-alleles where lacing is commonly seen are eb (brown) and ER (birchen). On the e-allele eb, lacing can occur with only Co/Pg/Ml, but on ER, Db is also required, as Co without Db on ER is not strong enough to restrict the high levels of eumelanin found on ER. Db, however, does restrict the eumelanin of ER and is thus required to create lacing on the birchen background allele. These are not, however, the only genes that Co and Db interact with. Co and Db also interact with Aph and Aph^I and their other interaction genes (s+/S, Mh, Di, ig, etc.)

The interactions of Co and Db with Aph and Aph^I are very fascinating. In short, Co interacts most strongly with sex-linked pheomelanin (s+ and/or S – the s-locus alleles), while Db interacts most strongly with Autosomal pheomelanin. However, we cannot leave it there, as there is more to these interactions than that one sentence can sum up.

First, let’s look at Co. Columbian, as stated above, interacts most strongly with sex-linked pheomelanin, and it is sex-linked pheomelanin that Co extends into the breast and body of both sexes on all the e-alleles it effects (e+, eb and eWh, but ER ONLY when Db is present, and E not at all). Regardless of whether we see Aph or Aph^I, it is the sex-linked pheomelanin that Co extends into the typically eumelanic areas. On red (s+) birds, it is very easy to see on the males. An example is some lines of Buff Brahma in which the males show a shoulder and top of head/around face/outer hackle edge much darker than the rest of the body, but the breast is as light, if not lighter, than the lower hackle. This means that even though Aph and Mh are present, the presence of Co (without Db) does not allow them to effect the breast. It is even easier to see in silver (S) examples.

We often see silver Columbian males that have a clean, snow white breast, yet the hackle, saddle and shoulder will be cream/yellow – ‘brassy’. The yellowing of these areas is the result of the presence of Aph, yet there is no effect on the breast, showing that Columbian extends sex-linked pheomelanin into the breast of these birds and completely restricts all expression of Aph on this area. A further example is that when Mahogany is present on a silver Columbian bird that has Aph instead of Aph^I, the result is a rooster with a clean white breast, yellow hackle and saddle and a Mahogany shoulder. Columbian thus restricts Aph from the breast, while extending sex-linked pheomelanin into the breast of the male.

The most desirable Silver Columbians are those that are homozygous for Aph^I, and have no Mahogany or other red intensifiers, as these will be a clean white silver. Further, when such genes as Dilute (Di) and/or cream (ig) are also present on these Aph^I silver Columbians, as we have discussed in previous articles on obtaining clean white silver plumage, the effect is magnified and we see none of the brassiness that even some good, clean lines show when exposed to sunlight.

However, this is not the end of the story for Columbian, because Columbian is often found with Db, and Db changes the game a bit. Before we look at the interaction of Db and Co, let us discuss Db.

Db is a very interesting gene and may actually be a major gene with one or more modifier genes, some of which may be linked, interacting to make what we think of as the typical Db expression of pheomelanic extension in both sexes. Dark brown is most commonly known from varieties such as ginger red, where it creates a warm tan-orange tone. However, Db can make other tones, depending on its interactions with such genes as Di or Mh. With Mh saturation, Db creates the typical Rhode Island Red phenotype and with the addition of one or more of the recessive black complex of factors, Db creates the exhibition form of Rhode Island Reds that might more appropriately be called “Rhode Island Near-Blacks”.

Dark Brown extends Autosomal pheomelanin into the breast area (as Co does with the s-locus alleles) and interacts most strongly with Aph/Aph^I. While Db does not extend the s-locus alleles, it does interact with sex-linked pheomelanin by changing the tone of s+ to a tan-orange, especially when Di is present and Mh isn’t present.

We can clearly see the effects of Db extending Aph (and by proxy Mh) into the breast, even when silver is present, in such varieties as the Red Shouldered Yokohama or some of the new color varieties of Serama known by various food-names (with no reference to their actual genetic components). There are very few standard varieties in the US that encompass Silver, Aph, Db and Mh. The Red Shouldered Yokohama being the only one I can easily think of (though this one is more complex than the simple S, Aph, Db, Mh combination discussed), but such combinations are seen in the standards of other countries and further, we often see this combination occurring in various landrace breeds (such as the Serama) as well as in various crossed birds where the color is marveled at as though it were some new spontaneous mutation (it isn’t!).

In these combinations, male birds that are homozygous for silver (on e+, eb, eWh or ER), but that have Aph (and no Aph^I), along with Db and Mh show a dark red breast, back edge of the lower wing feathers, shoulder and back, but the hackles, saddles and main wing feathers (the “duckwing” triangle) are cream to pale yellow. The females will vary a great deal more than the males depending on the e-allele, but will express red in the body with silver/cream/pale yellow hackles with exact distributions based on their respective e-allele. These phenotypes are only possible due to Db extending Aph and Mh into the breast/body of these birds. Since Columbian does not extend Aph into the breast, such phenotypes cannot be created using Co alone.

When Db occurs with S and Aph without Mh, the result is a bird that is entirely pale cream to light yellow throughout the body and hackles in both sexes, while the same combination but with s+ instead of S and ig will create a nearly identical phenotype. Db with s+, Aph, and Di without Mh creates the classic ‘Ginger Red’ phenotype. Add Mh to this and you get a slightly darker version of ‘Ginger Red’ that is more red and less tan or pumpkin. When there is Aph, Mh and no Di on red, we see the color of a typical Rhode Island Red and when recessive melanizers are added to that, we see the near black phenotype of the exhibition RIR. When Db occurs with Aph^I and S, we get a clean ‘Silver Ginger’, and the more dilution genes such as Di or ig that we add, the cleaner and whiter that silver will be. Without the diluters, S and Aph^I with Db will tend to be slightly brassy, but not the pale yellow of the same version with Aph instead of Aph^I.

Now to make things even more complicated and confusing, Co and Db can interact. There is not just one effect. The first effect one will note is that in regards to Pattern gene, Co overpowers Db and so when Co and Db are combined with Ml and Pg, the resulting pattern is a lace. Co and Db on the same bird with Aph but without Mh allows Co to have the greater effect on the tone of the pheomelanin, but with Aph and Mh, Db has the stronger effect and allows Mh to saturate the pheomelanin in a manner that Co alone would not allow. This can be seen in such varieties as black laced red (as opposed to black laced gold or “golden laced”), white laced red and blue laced red where Co is clearly present due to the laced pattern, but the pheomelanin is much darker than one would typically expect from Co alone. In that instance, Db allows Mh to extend into the pheomelanically extended areas to create the dark red visual effect. Some of the medium red lines of production RIR also have Columbian along with Mh and Db, though the show lines and darker production lines do not seem to have Co.

In the golden-laced varieties, Dilute (Di) plays a major role in lightening the tone to the bay color we expect. My tests show that all golden-laced birds (Sebright, Wyandotte and Polish) carry both Co and Db. Even when Mh and Aph are present in these cases, Co interacts with Di to allow the pheomelanin to be diluted to the golden tone, overpowering Mh and Aph and not allowing the expression of mahogany in the pheomelanin, except for partial expression on the male bird’s shoulder and the upper hackle/head of both sexes.

When S is present instead of s+, along with Co and Db, and Aph, we see brassy silver laced with the palest area being the pheomelanin of the breast, while the rest of the pheomelanic areas are a cream to pale yellow. To secure the cleanest white in silver laced varieties, Aph^I must be present and homozygous, whether Db is present or not. In instances where Mahogany and Aph are present on silver laced birds with both Co and Db, Mahogany is restricted and still does not influence the breast, as Co interacts with the sex-linked Silver (S) and has the greater influence, restricting Aph and Mahogany. If Aph^I is substituted for Aph in this last case, Mahogany does not express at all, as Aph is restricted and Mahogany requires Aph as a platform to express. The only effect of Mahogany in such an instance may be one or two red feathers in the shoulder of the male and a slightly darker brassy tone to the hackles and saddles, especially at the top of the head.

As you can see, the interactions of Aph and Aph^I with Db and Co are very complex and I hope my attempt here to explain some of these interactions has not caused you even more confusion. In the future, I hope to undertake a much more detailed description of these interactions, but for now, and the sake of brevity in an article, I hope this will give you a good point to begin to understand the many phenotypes that can emerge when dealing with the combination of many genes.

It is important to remember, also, that when dealing with heterozygotes, the visual expressions can be variable. To fully understand the results of various combinations, we must see them as homozygotes. However, most breeders out there who encounter such combinations will likely be seeing heterozygosity at various levels and this can make the expressions even harder to judge.
While the basic premise of Autosomal Pheomelanin and the Inhibitor of Autosomal Pheomelanin are fairly simple concepts and in practice are simple to recognize and work with, the fact that there are potentially many interaction genes means that this simple concept of Aph and Aph^I can seem very complicated and overwhelming. It is true that a multi-gene recombinant phenotype can be very hard to judge, especially when there is high heterozygosity at many alleles, but the most basic aspect, that of Aph and Aph^I, can be summed up very easily. All domestic fowl have Aph, just as all have sex-linked pheomelanin and eumelanin. In general, those birds with one dose of Aph^I will only show partial expression of Aph, while only those birds with homozygosity for Aph^I will not show any visual expression of Aph. The important thing to remember is that the expression of Aph will vary depending on the dosage effect of Aph^I and the other (potentially many) genes that are interacting with both Aph and Aph^I. It is these potential interactions that make this a complicated and often confusing subject.

The Expression of Autosomal Pheomelanin (Aph) and the Inhibitor of Autosomal Pheomelanin (Aph^I) on the common E-alleles (e+, eWh, eb, ER and E)

The Expression of Autosomal Pheomelanin (Aph) and the Inhibitor of Autosomal Pheomelanin (Aph^I) on the common E-alleles (e+, eWh, eb, ER and E)

Part 2 
Originally published October 2012 in Exhibition Poultry E-Zine


Brian Reeder

In this article, I will outline the effects of Autosomal pheomelanin and the Inhibitor of Autosomal pheomelanin on the five commonly encountered alleles of the e-locus.  It must be noted here, at the beginning of the article, that there are genes that interact with Aph and Aph^I beyond the e-alleles. Some of the most basic interaction factors were discussed in last month’s article ‘The Expression, Suppression and Interactions of Autosomal Pheomelanin (Aph) in the Domestic Fowl’, and include such factors as Mahogany, Dilute and cream. While this article will not deal with the other interaction genes (such as Columbian or Dark brown aka ‘ginger’), we will look at these factors in next month’s article. With that out of the way, let us continue on to discuss the e-locus interactions.

The five commonly seen e-alleles are e+ (duckwing), eb (brown), eWh (wheaten), ER (birchen) and E (extended black). Most simply stated, Autosomal pheomelanin is found on all of these alleles, though the distribution effect is somewhat different on each allele, most visibly on the females in several cases. The Inhibitor of Autosomal pheomelanin can also be found on, and express on, all of the e-alleles.

The males of all five e-alleles are much alike in their expression of Aph or Aph^I. There are subtle differences between the males of each allele that we will discuss below, but it is the females where Aph and/or Aph^I are often most visible and variable, and help to create the unique appearances that we most relate to the e-alleles.

As I stated in my article last month, I feel that Aph is found in all of the jungle fowls and that Aph^I is found in the gray jungle fowl and perhaps also in the green jungle fowl. Whether the form of Aph^I found in the gray jungle fowl is exactly the same as that found in the modern domestic fowl is not clear, but it is the likely source of Aph^I in the domestic fowl and if not the exact same gene is likely the precursor to Aph^I as described in domestic fowl, just as the yellow skin gene found in the gray jungle fowl is now thought to be the precursor to, and origin of, the yellow skin gene found in the domestic fowl.

The E-alleles
As we discuss the e-allele expressions of Aph and Aph^I, it is very important to bear in mind that I am discussing these alleles in their most basic expression. For example, E (extended black) is commonly thought of as a black chicken, but as I pointed out in my article two months ago on the genetics of black chickens, E, in and of itself, does not create a solid black chicken, and requires melanization factors to completely melanize an E-based bird to solid black. Thus, as I describe the interactions of E with Aph and Aph^I, I am discussing that allele without the extra modifiers. In other words, I am not discussing the melanized expression of E, the fully black bird, but am discussing the allele in its most basic state, where pheomelanin expresses in some parts. The same will be true for all of the other e-alleles. Our discussion for this article will be restricted to the e-allele with consideration of the s-allele and it’s most basic interaction genes (Dilute, cream), as well as Aph/Aph^I, and Mahogany (where applicable). We will not discuss any genes that were not part of last month’s article, beyond the e-alleles, in this article.

Duckwing (e+)

I have discussed the e-allele e+ at some length in two previous articles for Exhibition Poultry.  One was titled ‘Pigmentation of the Red Junglefowl’, and ran in the April 2011 edition while the second was titled ‘The Genetic Factors of Silver Phenotypes’ and ran in the December 2011 edition. For a detailed discussion of the interactions of the e-allele e+, the two s-allele mutations, and the Aph and Aph^I factors and modifiers, please refer back to those articles. For this article, I will stay with a simpler explanation, but strongly recommend you review these two previous articles in conjunction with this series.

The duckwing allele is characterized by the so-called “bb red” or black breasted red male, considered “duckwing” due to the triangular pheomelanic area of the folded lower wing. Regardless of the s-allele combination, the male retains the basic “black breasted whatever” format. The female is a combination of melanin, sex-linked and autosomal pheomelanin. Her brown back, orange hackles with a black center stripe and salmon breast characterize the female of this e-allele. The salmon breast, which is her most distinctive characteristic, is the main diagnostic trait of the duckwing female.

The male of the duckwing allele differs little from the males of the e-alleles eb and eWh. The only major variation between the e+ male and the males of ER and E is the presence of the pheomelanic wing triangle, which is absent on the solid black lower wing of the alleles E and ER. It is the female where there is a great difference from the other alleles of the e-locus.

Autosomal pheomelanin has the greatest expression in the male of the e+ allele on the shoulder and back, the outer edges of the main wing feathers, the top of the head around the face and around the outer ring of the hackles and along the back edge of the saddles. The remaining pheomelanic areas are predominantly sex-linked pheomelanin. In the female, the breast is predominantly autosomal pheomelanin, while the back, wing, cushion and secondary tail feathers are a blending of sex-linked pheomelanin, autosomal pheomelanin and eumelanin. The hackle of the female is predominantly sex-linked pheomelanin with the upper head, area around the face and the outer edge of the hackle strongly influenced by Aph, just as in the male.

When silver (S) is the gene at the s-allele, the sex-linked pheomelanic areas are lightened to a cream-yellow tone, but the autosomal pheomelanin is unaffected. Thus silver hens show the strongly salmon breast, and if mahogany is present, the breast, back and shoulders may be deep reddish brown, just as the shoulder of the silver male can be dark reddish brown with mahogany present in conjunction with silver and Aph. Aph^I is required to block the expression of autosomal pheomelanin (and thus also Mahogany) and begin to work toward a fully clean white silver phenotype.

When hens are heterozygous for Aph^I, the breast can be patchy, showing salmon areas and cream areas, sometimes as slight lacing of cream on the salmon breast feathers, and sometimes as patches of cream or even a central area of cream in the center of the salmon breast. Fully homozygous hens for Aph^I show very little color in the breast, with the breast tending toward cream/beige with very little salmon tone at all. While these hens will have a lighter tone of cream with S (Silver), even the s+ (red) hens show a very pale breast of a beige tone when Aph^I is homozygous.

Brown (eb)

On the brown allele, eb, the males are nearly identical to the males of e+, except that they will tend to have more distinctly striped hackles and saddles, and Aph has a somewhat stronger effect on the upper hackle and along the outer edge of the main wing feathers and outer edge of the saddle, than is seen in the e+ male. This is a very subtle point, as males of both alleles show Aph saturation in these areas. In the eb male, it is only slightly stronger in saturation. Otherwise, the males are identical.

The females, however, are another story. In the most basic sense, the major difference between the e+ female and the eb female is the later lacks the salmon breast of the former. The breast of the eb hen is replaced with a combination of the three pigments, just as in the back of the e+ hen. So we can state that he entire body of the eb hen is very similar to the back of the e+ hen. The eb hen’s entire body plumage behaves as the back of the e+ hen also. As the eb hen’s back is a blending of sex-linked pheomelanin, autosomal pheomelanin and eumelanin, we can produce the same range of shades as seen in the e+ hen’s back. For instance, if we have s+ (gold or red) and Aph with mahogany, we see a very dark red-brown body as seen in the Partridge and dark brown varieties. 

If we change s+ to S (silver) and have Aph^I, we get a very clean silver-gray background as we see in the cleanest silver penciled varieties. When we have silver without Aph^I and rather have Aph present, we see a silver hen that is not the clean, crisp black and white of the best silver penciled, but rather the entire body shows a slightly cream tinted under color, sort of like a tobacco stain on white, which is commonly seen in many less clean silver penciled lines. The genetically identical male of this type will also show a yellowish tone to his pheomelanic areas and we call such lines “brassy” in exhibition terms. To get the very clean, crisp “black and white” silver penciled expression, the inhibitor of autosomal pheomelanin is necessary along with silver.

With the eb allele, there is a reduction of the expression of autosomal pheomelanin in the female, while there is an increase in the expression of eumelanin and sex-linked pheomelanin, as compared to the duckwing allele, e+.

Wheaten (eWh)

I would consider the allele eWh, wheaten, to be the opposite of eb, in that it is a reduction of eumelanin and sex-linked pheomelanin as compared to the allele e+, duckwing.

There is little difference visually between the males of e+, eb and eWh. The wheaten males tend to show less (and often none) of the melanization striping in the hackle and saddle, while Aph has a greater saturation in all of the pheomelanic areas. This is especially noticeable when S (silver) is present at the s-allele (even more so when Mahogany is also present), as Aph clearly suffuses all pheomelanic areas more fully and with stronger saturation as compared to either e+ or eb. This some silver wheaten males can show a considerable amount of salmon to dark red coloring in the cream to silver hackle, which can be very confusing if you are not clear to the effects of Aph on eWh.

The eWh hens are the opposite of the eb hens, in that they show a reduction of eumelanin and sex-linked pheomelanin and an increase in autosomal pheomelanin. In short, the entire body of the eWh hen is similar to the breast of the e+ hen, while the blending of eumelanin, sex-linked and autosomal pheomelanin, as seen on the back of the e+ hen and the entire body of the eb hen, is not present on the eWh hen.

At the darkest end of the spectrum, when we see s+ with Aph, Mahogany and melanization on the eWh female, the entire body tends to be a dark brown/salmon tone often called cinnamon, as in the Cubalaya. Without the melanization saturation, we see the normal wheaten female where the entire body is salmon colored, as seen in Malay or some Old English Games. When the wheaten hen is heterozygous for Aph^I, we see a split between the back/upper body and the breast/lower body, where the back is salmon, but the breast is cream colored. With the Aph^I homozygote, the entire body of the wheaten hen is cream colored, as we see in Some Old English Game Bantams that show this very pale form of wheaten.

The addition of silver does not change the expression of Aph/Aph^I in the body of the wheaten hen (as described in the paragraph above). The only major change from silver to the wheaten hen is in the hackle, where the silver gene lightens the hackles from cream to white, depending on the other genes present. However, as I described above for the male of the wheaten allele, the females also show a stronger saturation of Aph in the hackles, especially when Mahogany is present. Thus, one can have a silver wheaten female and still see a good deal of dark red in the otherwise cream colored hackle (some Salmon Faverolle hens show this effect, for example), if Aph is present. The cleanest, palest and most colorless wheaten hens are found when wheaten is combined with silver and is homozygous for Aph^I. Such hens are a solid, pale cream to white color with a bit of black in tail, wing and hackle and can easily be confused with the silver Columbian variety (of which the standard form is on the e-allele eb).

Birchen (ER)

The male of the Birchen allele is very similar to the males of the preceding e-alleles, except that he does not show the pheomelanic wing triangle, has very strong hackle and saddle center stripes and does show a pheomelanic lace at the edge of his breast feathers. This breast lacing is the major diagnostic factor (along with chick down) to distinguish ER from E. The male of the ER allele shows the same effects from Aph and Aph^I as the e+ male and in the same regions. The breast lace is generally dictated by sex-linked pheomelanin though, and this differs from e+. As well, the black wing will show no effect from Aph or Aph^I, due to the full melanization caused by this e-allele.

The female of the ER allele is nearly identical to the male, except that she does not have a pheomelanic shoulder or saddle. She is basically fully eumelanic (black) with a pheomelanic hackle with black stripe and pheomelanic lacing on the black breast. On this allele, the strongest effect of Aph is on the head, upper hackle and edge of hackle, as seen in the hens of other alleles. The breast lace of the female is also determined by sex-linked pheomelanin.

Only when other genes, such as Dark Brown (Db – aka ‘ginger’) or Db with Columbian are added to this allele, does the effects of Aph or Aph^I become noticeable. While Aph and Aph^I have little visible effect on the unmodified form of the ER allele, either (or both) of these factors can be present and can show their effects when ER birds are crossed out to birds of any of the previous e-alleles or when other modifier genes are present.

Extended Black (E)

Extended Black here does not refer to a solid black chicken. In fact, the phenotype on un-melanized E is nearly identical to ER, except that there will be no breast lace in either sex and the hackles/saddles will show even heavier melanic striping than in ER.  The effects of Aph and Aph^I is the same on E as on ER: minimal. The male will show the effects of Aph in the same areas as all the proceeding males, while the females will only show the effects on her head, upper hackle and the outer ring of the hackles, as in the proceeding females. One major difference between E and ER is that while ER can show the effects of Aph and Aph^I when modifier genes such as Db and Co are present, E is not effected by Co or Db and thus does not show the effects of Aph or Aph^I when either of those modifications are present. However, all E birds carry Aph and/or Aph^I, and so it is a consideration when outcrossing the other alleles to this allele, if in no other case.