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
By
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.
