Wednesday, February 26, 2014

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.