Tuesday, January 29, 2013

Blue Genes? Chicken Genetics Made (almost) Simple

By: Karen - KI4GOT   (Visit Karen’s Farm Here)

Chicken genetics seem to be an endless source of confusion for so many people. I've taken a number of genetics courses in college, and at first they even confused me, but I also didn't know much about what the various mutations looked like in comparison to a number of different breeds. When I first started keeping chickens again, I had no idea where to start in determining what mutations were involved in some of the varieties I had.

Since then, I've done more research into specific colorations found in certain breeds, such as Bantam Cochins and Dorkings, and have gained a greater understanding of what goes into each variety. It also doesn't help that the same color in one breed may be called something else entirely in another. For example, comparing Brahma's to Cochins, a Light Brahma is also known as Columbian in the Cochins, while a Dark Brahma is known as Silver Penciled in the Cochins. Silver Grey dorkings are known as Silver Duckwing in many varieties, Red Dorkings are also called Black Breasted Red (aka BBR), or Red Duckwing in other breeds.

Before I start, let me mention that I tend to refer to mutations as having 1 or 2 copies of the gene, while the description below mentions each gene having 2 alleles. This is just 2 ways of saying the same thing. Here's a brief review of what DNA is.

Living things are made of millions of tiny self-contained components called cells. Inside of each cell are long and complex molecules called DNA. DNA stores information that tells the cells how to create that living thing. Parts of this information that tell how to make one small part or characteristic of the living thing – red hair, or blue eyes, or a tendency to be tall – are known as genes.

Every cell in the same living thing has the same DNA, but only some of it is used in each cell. For instance, some genes that tell how to make parts of the liver are switched off in the brain. What genes are used can also change over time. For instance, a lot of genes are used by a child early in pregnancy that are not used later.

A living thing has two copies of each gene, one from its mother, and one from its father. There can be multiple types of each gene, which give different instructions: one version might cause a person to have blue eyes, another might cause them to have brown. These different versions are known as alleles of the gene.

Since a living thing has two copies of each gene, it can have two different alleles of it at the same time. Often, one allele will be dominant, meaning that the living thing looks and acts as if it had only that one allele. The unexpressed allele is called recessive. In other cases, you end up with something in between the two possibilities. In that case, the two alleles are called co-dominant or incompletely dominant.

There are two types of mutations. Autosomal and Sex-linked. All the mutations known in chickens are autosomal, with the exception, for all mammals and birds, of one pair of sex-determining genes. In people, men are shown as X/Y, while women are X/X. In poultry, the hen is designated as X/- while the rooster would be X/X. Each parent donates 1 allele from each gene in the DNA strand. Only the X chromosome carries genetic information, the /Y or /- sex determining chromosome does not carry any other information.

There are so many mutations and so many breeds, it can be overwhelming to say the least. It also doesn't help that a number of mutations react differently when combined with others. What I'd like to do here is to explain the basic functions of some types of mutations...

**NOTE: When you see a mutation abbreviation with + next to it, that refers to the normal or wild type gene that is not affected by any mutation. Essentially, a Black Breasted Red is unaffected by any mutations at all. It is the coloration found in the original Jungle Fowl that chickens descended from. Mutations shown capitalized are considered dominant, while lower case letters are recessive. Sometimes there are multiple mutations found on the same gene, and even though several might be recessive, there is a dominance of one over another.

Recessive mutations always require 2 copies of the gene (aka matching alleles) to be visible, while dominant mutations only require 1 copy to be present for the mutation to be apparent. There are also dominant mutations that are known as 'incompletely dominant', where only 1 copy of the gene gives you one visual type while 2 copies gives you another.

The mutations known to chickens typically do one of three things. They affect pattern, red pigmentation (known as pheomelanin) and black pigmentation (known as eumelanin). The pattern genes can be some of the most confusing, so I will leave that for last. Some mutations affect roosters and hens differently.

Kippenjungle's Chicken Calculator is a handy tool for anyone wanting to learn how genes interact with each other. All pictures (other than photos) below are from there and show only the single gene effect on an otherwise wild type bird. Another note - although the images are basically the same for some mutations, there are slight differences when shown on a live bird. These images are just to give you the basic idea of what it does.
For the most part, pheomelanin and eumelanin are affected in one of 2 ways. They are either enhanced (made darker) or restricted (made lighter).

These mutations are:

· Mahogany (Mh) - dominant, enhances red but limits some black.
· Dilute (Di) - dominant, dilutes red and gold pigments.
· Champagne Blond (Cb) - dominant, dilutes gold pigments.
· Inhibitor of Gold (ig) - recessive, changes gold pigments to yellow (lemon).
· Silver (S) - sex-linked incompletely dominant, turns red to white in roosters and turns brown to grey and lightens the salmon breast (when present) in hens.
· Dark Brown (Db) - refers to color of chick down. Columbian-like restrictor of black. Less effective on hens. Reacts with other mutations to cause some patterns and acts under Birchen.
· Melanotic (Ml) - dominant, enhances black pigments. Also shifts black pigment helping form patterns in the presence of other genes.
· Charcoal (cha) - recessive black enhancer.
· Chocolate (choc) - sex-linked recessive, dilutes black pattern to chocolate color.
· Dominant White (I) - dilutes black patterns to white (sometimes leaky).
· Dun (Id) - incomplete dominant. 1 copy dilutes black to brown, 2 copies dilute further to khaki.
· Smokey (is) - recessive blue. changes the effects of dominant white to a blue color. recessive to wild type i+
· Blue (Bl) - incompletely dominant, 1 copy dilutes black to blue/grey, 2 copies dilute further to splash.
· Recessive White (c) - no expression of any color, thus white feathers.
· Lavender (lav) - recessive, dilutes black to lavender, dilutes gold to isabell. The American Poultry Association (APA) refers to the lavender color as "Self Blue".
Pattern genes are complex and often confusing. They may simply change the coloration of each feather, only certain areas of a bird or even areas only on a single sex. Quite often they also respond differently in the presence of other restricting or enhancing mutations listed above.

The e-locus mutations are sometimes the hardest to understand, since many affect each sex differently. They may also modify (or be modified by) other genes present.

· Wild Type (e+) - Males black breasted with red duckwing (wing triangle), hackle, saddle, shoulders. Females brown-gold with salmon breast, black stippling on back and black tail.
· Extended Black (E) - Dominant, turns the wing triangle black, changing it from a duckwing to a crow-wing. Males become a rusty black, hens less rusty black.
· Birchen (ER) - Turns wing triangle black (crow-wing) but leaves hackle and saddles normally marked. Black breast can be laced. Somewhat flattens red tints.
· Wheaten (eWh) - Least permissive for black, most permissive for red. Males are wild type without hackle black, females wheaten colored without salmon breast and almost no stippling on back.
· Partridge (eb) - Males are wildtype but somewhat heavier black striping in hackle. Hens are wildtype but without salmon breast. (Not to be confused with the color Partridge, in which hens are double laced)
The mutations affecting feather patterns are probably the easiest to understand (at least for me).

· Columbian (Co) - restricts black from the body of both males and females, also suppressing the salmon breast in hens. leaving the hackle pattern and black tails. Does not have any effect on ER (birchen) birds.
· Pattern gene (Pg) - changes the black pigment in hens to concentric penciling, males remaining unchanged except in the presence of certain other genes.
· Barred (B) - sex-linked dominant. produces alternating bars of black and white pigment. Males with 2 copies of the gene will appear lighter and the barring finer and more distinct, where males with only 1 copy will resemble females with wider and less distinct barring (sometimes darker overall coloration).
· Mottled (mo) - recessive, giving white feather tips or less regular white patches.
When you start combining certain mutations you can get some drastic differences from what you might expect, and some different combinations produce nearly the same result.

· Co, Pg, Ml - single lacing
· Co, Ml - quail-type pattern, columbian with patterned back

· Pg, Ml - double laced
· Db, Pg, Ml - spangling
· Db, Pg - autosomal barring (quilt pattern)
· Co, Db, Pg, Ml - single lacing (sometimes half moon spangling) with patterned tail
· Co, Db, Ml - quail-type pattern, columbian with patterned back
· Db, Ml - quail-type pattern, columbian with patterned back
· Co, Pg - incomplete single lacing

I should also mention though, all of the talk of colors has NOTHING to do with breed requirements in regards to type or conformation. For more information on specific breed requirements I recommend purchasing the APA Standard of Perfection, available directly from the APA at http://www.amerpoultryassn.com/store.htm

Here are a few other examples of a few patterns and combinations, including some not mentioned above, that you might find when dealing with laced varieties.
Also included are a few pictures of REAL birds, to give an idea of some of the colors listed above...
Leigh's Blue and Splash Swedish Flower Hens. These birds have the blue gene (Bl/bl on the left, Bl/Bl on the right), in addition to mottling (Mo) and columbian (Co) that give the typical calico/mille fleur pattern.

My own blue laced red bantam Wyandotte rooster and a splash laced red Wyandotte (LF) pullet. The mutations involved in these birds involves the pattern gene (Pg), melanizing (Ml) and columbian (Co) which give the classic lacing, plus blue (Bl/bl for the roo & Bl/Bl for the hen) and Mahogany (Mh) to deepen the intensity of the red.

This next pair are both Red Dorkings, essentially the wild type of chickens, having no mutations at all.

The three birds in the foreground are silver grey Dorkings (two hens on the left, rooster on the right). The only mutation involved in these birds is silver (S). To the right (chopped off a bit) and also the picture below are two dilute red Dorkings. I'm not positive of the exact genome, but these two girls have dilute (Di) and the one below may possibly also have mahogany (Mh), which would explain the darker red head and breast than the one above.


Sunday, January 27, 2013

Chick Health: Is It Splay / Spraddle Leg, Or Something More?

"Texas" Asks:

I had two chicks hatch yesterday. They were local eggs and I kept the humidity much higher than my first two tries at incubating. The first one hatched at the end of day 20. It had some of the egg white still in the eggshell. In fact, it carried around a little bit of shell after it hatched. The second hatched on day 21 and had much less of the white.

I left the two in the incubator overnight. I kind of thought chick #2 had a leg problem, but wasn't completely sure until this morning. Here are some pictures. I am not sure if this is spraddle/splay leg or a slipped tendon. I have tried to pull the tendon back into place, but it doesn't seem to give. I am putting pressure on it until the chick squeaks.

In the "natural" position.

The leg that is not in the correct position.


("Texas" then carefully followed directions for correction of Splay / Spraddle Leg, making a brace from a band-aid.)

Chrissy in CA Writes:

Is this baby chick getting around/up walking, using the bad leg and it's foot correctly yet?

If there is no improvement within a couple of days with the brace/hobble on, I have a different idea on what the leg issue could be...

"Texas" Replies:

Would love to hear what you think might be going on. It is not really walking or putting pressure on the foot. The leg is straightened out now, but it doesn't grasp with the foot.

Chrissy in CA Writes:

I was hoping the chick had improved and was zipping around the brooder tripping over it's hobble/brace, by now. I hate being the bearer of bad news...

Judging by how the entire leg looks twisted to me, my suspicion is a rotated femur (which is a deformity, not an injury).

While I am far from a hatching expert, I have incubated a lot of eggs (Guinea, Turkey, Quail, Silkie), hatched out well over 1700 birds... so I've run the gamut of incubator issues and hatcher injuries etc but in my experience with splayed leg (or legs), the leg doesn't turn out from the body. Normally splayed legs are the result of an injury cause by slipping/poor footing which results in a wobbled out/stretched out joint socket that lets the leg slide out from under the body to the side, no rotation of the entire leg is involved. Usually within a couple hours of being braced/hobbled (and the chick or keet has gotten used to the hobble) the leg is used normally, with no favoring, no pain. 
You mentioned slipped tendon, and the tendon not budging when you tried to move it... I can definitely see in your pics that the tendon on that leg is not in the correct position over the back of the hock. If it was a slipped tendon it would be easily moved back into the tendon groove (but would probably slip right back out as soon as the leg was bent), which with my suspicion of a rotated femur would be a resulting deformity that occurred during development while still in the egg (not from an injury after hatching).

The chick is most likely not grasping with that foot because the femur rotation and tendon deformity are causing it considerable pain. Hopefully I am wrong, but as I mentioned splayed leg is a pretty quick fix if noticed and the legs are braced/hobbled soon enough... which in my opinion you did.

Sadly, Texas did have to cull this chick as a result of its rotated femur. Our sincere Thanks goes to "Texas" and Chrissy in CA for sharing this learning experience with us!