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
By
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.
