Monday, April 22, 2019

Fantailed Chickens

Fantailed Chickens

The full fantail as seen on a Serama rooster from the back view. You can see that all the changes from wild type associated with the fantail phenotype are present such as high tail angle, left and right tail segment orientation shifted to open and flattened, feather orientation readjusted to run with the plane of the tail and permanently spread (fanned) tail segments. This was not a pose. His tail was like this all the time.

This blog post looks at a few fantailed birds, some from well-known breeds, some from more obscure breeds and others are birds that I have had or produced.

Fantailed Langshan showing an extreme fanned tail. This type of tail os considered 'non-standard' to Langshan breeders, but they occur in most lines, indicating recessive genes at work that are carried by birds showing the standard tail. However, it must be pointed out that the standard Langshan tail still shows several of the fantailed traits - High tail angle, tail segments opened at the base and individual feather orientation modifications. It is only a step or two from the standard Landshan tail tot he fully fantailed form, mainly a further shift in individual feather orientation and further flattening (opening) of the two individual tail segments. The standard Langshan tail form can be called a vase-shaped tail, while the bird above shows a fan-shaped tail. The later is simply a more extreme (further modified) version of the former. Side view of the same male below.

This male Cochin tail is a fan-shaped tail over a large amount of fluff positioned below the fan-shaped tail. This was a "dark" phenotype, being a melanized Partridge on the eb (brown) e-allele, which I received with some Partridge chicks. An effort had been made to improve the type of the Partridge by going out to some of the best black lines, so the recessive melanizers appeared in those lines for a long time afterward. The type of these "dark" birds were greatly improved over the original Partridge line, and very nice Partridge also came from that work. I was lucky enough to get a pair of these to work with from 5 Partridge chicks I received. These two showed both high disease resistance and good vigor. The male (pictured above) by chance showed several of the fantail traits, as do many of the Asiatics such as Cochins, Brahmas, Langshan and Silkie. The hen (pictured below) had a fairly normal, pinched tail, though at a slightly higher tail angle than in the wild type. She had the normal cochin fluff and her tail had the look I associate with hatchery lines of Cochins. She was a remarkable bird though, with many fine traits and an excellent breeder.

Exhibition Cochin Bantams showing the wide spread, laterally flattened tail form over the large amount of under fluff common to exhibition lines. These fanned tails are at a lower angle than those seen in Serama or Langshan, because the breed standard for Cochin calls for a somewhat lower tail angle.

I have not bred chickens since 2012. I have been breeding pigeons since 2015. I am finding the pigeons to be a much better fit for my current housing limitations. In my breeding work with pigeons I am also focusing on fantailed phenotypes. I hope to compare the expression of the genes for fanned tail in chickens with those in the pigeon. This affords me the opportunity to make comparative observations of the identical phenotype in another genus.

Ginger red Silkie male showing a wide opened tail spread, again filled with the heavy fluff as in the Cochins above.

Enjoy the fantails shown in this blog! I will have more to say about the phenotype and the apparent genetic factors that lie behind it in several upcoming blogs.

First generation  cross of the "dark" Cochin hen (see above) x Dark Brahma male. In this instance, the male Brahma I had showed a partial fantail. This first generation male shows a full fantail, with short feathering and at a moderately high tail angle. 

A Serama showing a substantially open fanned tail. This one has full spread across the back of the tail, with the view from the back only being slightly cupped.

A New Hampshire bantam male showing a spread tail that is quite opened from side to side as seen from the back. The tail angle is only just above horizontal. The fanned tail can occur at any tail angle, as we see in the Cubalaya where the fanned tail at a low angle is called a "lobster claw" tail.

This picture from Barry Koffler's Feathersite shows a Ma Lai bantam from Vietnam, translated as "Hand Fantail" (the tail is said to look like a hand held up and spread like a fan). In this hen-feathered cock bird we see all the traits combined - High tail angle, left and right tail segment orientation opened, feather orientation turned to flatten the feathers and permanently spread (fanned) tail segments. This is the only breed I know of that is specifically selected for the fanned tail.

A photo of a stunning Japanese Satsuma-dori by Uichiro Sakamoto, taken from the internet for educational and comparative purposes. This breed often shows fanned tails, especially in the red-black variety. This is a lovely fanned tail at a lower angle. Many Oriental Games show a tail like this, though often less glorious than in the Satsuma. The Satsuma is the only other breed I know of in which the fanned tail is acknowledged and not selected against. I suspect there may be other obscure breeds that show the trait as a major positively-selected phenotype trait. However, it seems to be fairly common in a number of exhibition breeds where partial expression of some of the traits involved, making fuller, rounder tails. Chabo (Japanese bantam), Cochin, Serama, Brahma, Langshan, Cubalaya, as well as within descendants from the Asiatics such as Rhode Island Red, New Hampshire, Rock and Wyandotte breeds. Even modern commercial sex-links can show some of the traits associated with fantails when they have descent from Rock and New Hampshire or Rhode Island Red. I have even seen partial fantail traits in Cornish/Rock cross commercial meat birds, again, due to their descent from Rocks, which in turn descend from the old fashioned Cochin-China fowl of the 1840s, as do so many of the other breeds I have mentioned above. 

A Barred Plymouth Rock bantam hen showing a fanned tail where each side of the tail is spread, but the orientation of the two tail segments is only open at the base, and not completely spread out into the visually flattened tail when viewed from behind. Tails like this are much more common than the full fan tails, and such birds are usefully in a breeding program for the full fantails. The Asiatics are the common source for the fanned tail - including the Cochin family, the Oriental Games and Asian bantams. The Plymouth Rock descends directly from imported Chittagong/Cochin type birds crossed onto local barred stocks in the Northeast of the US in the mid to late 1800s.

A Golden Sebright rooster showing a wide fanned tail, but presented as two separate segments side-by-side. The tail angle is fairly high. As viewed from behind, this tail was two separate fans that touched each other at the top and were spread apart about fifteen to twenty degrees at the base. So this bird shows the high tail angle and the feathers fanned within the two segments, but it lacks the opened tail that turns the two tail segments into one wide fan, and it lacks the factor that turns the feathers into a plane of orientation with the opened tail. This is still a lovely tail, and is a fanned tail but does not represent all the genetic changes from wild type that exemplify the most extreme versions that mimic a fantailed pigeon, or a turkey or peacock with tail or train spread.

Another example of the tail as two separate segments, with each segment fanned and spread wide. This is the same type of tail as seen in the picture above of the Sebright rooster. This hen had a fairly closed tail though, when viewed from behind, with very little opening at the bottom of the two tail segments as viewed from behind the bird. We see such tails fairly frequently in a great many breeds and these traits are part of the full fantailed phenotype, so they can be used in breeding toward true fanned tails.

From this point on, all the pictures represent birds from my own breeding program. These birds are later-generation blends of multiple family lines. Their ancestry includes the Serama male at the top of the page, as well as the large fowl "Dark" Cochins and Dark Brahma line mentioned above. Interestingly, these lines shown below do not include any Langshan ancestry. They also include several lines of Phoenix, as well as Silkie and several other bantam components such as New Hampshire and Buff Rock bantams. There are other breeds in the ancestry as well from large fowl breeds, such as Golden Wyandotte and red/white sex-links.

Partially fanned tail in a Cochin/Phoenix F1 rooster. Very attractive and fairly open at the bottom from behind, perhaps 100 degrees in spread at the bottom feathers when fully extended.

Full sibling to the rooster above, and also showing a partially fanned tail. Cochin/Phoenix cross. The hen behind him is a select individual bird from commercial red/white sex-links. She was an exceptional layer, extremely disease resistant and of gentle disposition. Her tail also shows a partial opening from behind at the bottom of each tail segment with the top only touching along the upper webbing of the first feathers at the top on each side of the segments.

A later-generation blend of multiple breeds from my own breeding program, granddaughters of the two birds in the picture directly above (Cochin/Phoenix F1 male x red/white sex-link hen), showing a tail as two segments that are partially open at the base while touching at the top and each segment fanned. This hen produced offspring showing the fully fanned fantails. 

Son from the hens above showing a much wider opening at the base of the two tail segments, along with the fanning of each segment.

Another son of the hen above showing the fully spread tail with all four traits - high tail angle, left and right tail segment orientation opened, feather orientation turned in socket to make a smooth, flattened spread and permanently spread out (fanned) tail segments.

A view of the male above from behind showing the visual effect of the fully fanned tail. This tail form is static in this type.  It does not close. This is the way the tail looks all the time. Even when the bird is perching on a branch, the tail may close a bit in balancing, but never closes beyond about 60 degrees in openness. In the picture at the top of this blog, the Serama male is shown perched on a bamboo pole. Even perching there, where the tail is used as part of the ballast to create balance for the bird on the perch, the tail doesn't really close very much at all. 

Same rooster again, this time as a mature bird.

A daughter of the male above showing partial fanning. Fanning seems to be easier to achieve in males than in females. Once it is set in the females of a line though, it seems to reproduce consistently.

This is the son of the hen just above, from the partially crested male two pictures above. He shows much better tail fanning than either parent, though they each express some of the genes and carry the others that make the full phenotype. A cockerel in this picture, the tail was longer in the adult bird. Note how the individual main tail feathers are turned in comparison to wild type feathers, and also note how the sickles are coming over the fanned main tail feathers lying flat, showing that they are turned in orientation as well. In the full phenotype, the main tail feathers, the sickles and secondaries turn to lie in orientation with the tail. I have seen intermediate types where the tail is fanned, but the feathers are not turned and they look like individual blades, with edges oriented to sky and ground. These types do not give the nice, clean effect of the turned feathers in the spread tail creating the 'fan' form.

A daughter of the hen above backcrossed to her father, showing a partial fan where the two sides of the tail are well spread and there is some opening at the base of the tail. The spread of the individual segments is impressive though, and the tail consists of seven main tail feathers and a main sickle on both sides. Multiple feathering is a major breed trait of fantailed pigeon. Many of the exhibition breeds where fantails and their component parts can be found exploit multiple feathering in the tails to produce fuller effects. Most Asiatics (Cochin/Langshan/Brahma) will tend toward multiple feathering.

A cockerel, full brother to the pullet just above, a cross from the red and white hen back to her fantailed father. This male shows several of the genes making up the full fanned tail, but not all of them. The open fan is missing in this bird. However, you can see the turned feathers, cascading back and across the turned main tail feathers. Multiple feathering is apparent, as is the lift of the tail. The tail is fairly open across the lower back, at about 90 degrees. 

Full brother, but one year younger, to the cockerel above, fanned tail showing most of the traits, but lacking the completely flattened tail segments. 

Full brother to the cockerel above, a young cockerel, showing a nice fantail.

Two sibling cockerels from behind. These tails can take a full two years to fully mature. Their father, the most extreme fantail I raised to maturity, was less extreme in his first year (picture below). Langshan, Cochin and Brahma tend to take a couple of years to grow into their full feathering, and this line was the same in taking two years to mature. Bantams didn't seem to take two years to grow in, and Serama showing this tail type are sometimes quite extreme from an early age.

Come back to read more blogs on this phenotype. We will be looking at a host of subjects in relation to the fantailed chickens in subsequent posts. To keep track of this series, bookmark the main page for the series, of which this is the first post. Enjoy the pictures! I hope they whet your appetite for more. 

Next Page

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.