Black sheep & genetics - Page 1

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AandA

by AandA on 06 February 2008 - 09:02

Driving to work this morning past a field of sheep I noticed there was the classic single black one amongst a flock of about 50-60.

Which got me thinking, how does genetics explain this & does anything similar occur within the world of GSDs?

AandA


jc.carroll

by jc.carroll on 06 February 2008 - 13:02

Genetically the process is almost identical, though visually they couldn't be more different.

Similar things occure all the time with the GSD

Traditionally people tend to think of a color that looks white as always being a recessive trait. The white in sheep is actually an agouti pattern carried on the A-locus. Agouti (or "Sable" in GSD terms) is a dominant pattern. Different modifiers in the A-series control the base pattern of the white sheep: solid, wtih greying, badger-faced, and so on. Black is a pure recessive trait in sheep, still carried at the A. For a sheep to be black it must receive resessive black from both its white parents: Aw/Aw.

Sable is the dominant coat in the GSD, though the dog may carry other recessive patterns that go unexpressed. Black is a recessive that is only expressed when both parents are black carriers.

Using a GSD comparison, the black sheep in the field would be akin to the lone black GSD puppy in a tumbling pile of sable littermates.

 

(Basic Sheep Genetics)

http://www.shaltzfarm.com/shcolprim.html

http://www2.localaccess.com/primolana/page3.htm

 


AandA

by AandA on 06 February 2008 - 13:02

Thanks for the reply, but please bear with me as I have couple of follow up questions:

Am I correct in assuming recessive genes aren't just limited to colour? Although this may well be the most easily seen example, recessives can act in the same way with other aspects i.e. ear carriage, teeth count etc

Is there anything that determines which recessive a particular animal may carry or is it just good old mother nature stirring the mix?

AandA


Ceph

by Ceph on 06 February 2008 - 14:02

Theres usually a general ratio that geneticists follow for the way genes split during meiosis to guess things - however, according to mendel's laws they really just kind of randomly split.  You see it less in multiple baby breeds like dogs and pigs and more in single/twin baby breeds like sheep and horses - because oftentimes you wont get what you are looking for.

I have my Sheep production notes dinking around here somewhere...lol - there are some interesting alleles there that cause sheep like Suffolks (black legs, white fleece), white sheep (dorsets) and brown or black sheep.  Alot of the hair sheep crossed with normal fleece sheep end up a really nifty dark brown color.

~Cate


Sunsilver

by Sunsilver on 06 February 2008 - 14:02

Yes, recessive genes determine a great number of traits, some of them not easily seen. The long coat gene is another good example of a recessive in the GSD.

The parents, and chance, are the determiners of what genes a puppy receives.

Let's take the above example: two sable parents, both heterozygous for the sable gene (meaning they both carry the black recessives) statistically will produce 75% sable pups and 25% black. Suppose one of the parents is black: ww. That raises the chances to 50%, and all the sable pups will carry the black gene.

It looks like this, for ww (black) mated with Ww (sable, but heterozygous for the black gene)

         w            w

W   Ww         Ww

w    ww          ww|

 

Then of course, there's something called LINKED GENES that can throw a monkey wrench into the works. Let's say we have 2 genes that are on the same chromosome. As you know, chromosomes come in pairs, one received from the father at conception, and one from the mother. During the reduction division which occurs during the formation of the sperm and egg cells, the chromosome pairs separate.

                      ><

                      ><             (pairs of chromosomes lined up along middle of cell nucleus, as cell prepares)

                 ><              to divide.)

 

             <          >          (chromosome pairs separate, one going to each side of

            <           >           the cell, which then splits to form 2 new cells with 1/2 the

            <          >            number of chromosomes.)

 

So, let's imagine in that first pair of chromosomes, we have a gene for blue eye colour situated half-way down the chromosome. Very close to it, is a gene for long hair. Both traits are dominant, meaning if they are present, they will be expressed. (This is a made-up example, I don't have a real life one.) These genes will ALWAYS occur together, because they are on the same chromosome, and cannot separate. They are therefore referred to as linked genes. In this imaginary species, a blue-eyed animal will always have long hair.


jc.carroll

by jc.carroll on 06 February 2008 - 15:02

No problem, I love talking genetics. Genes control EVERYTHING about an organism. *grins* I'll try and keep from getting too technical.

Every organism (plant, animal, simple and complex) has a set of rules that dictate what it becomes.

Looking at people, there are only 23 chromosome pairs that dictate everything about our genotype (genetic structure), which in turn dictates our phenotype (physical structure). The "genome" is the full set of chomosomes for an organism, the entire basis for all inheritable traits of that organism. It is coded by DNA. The "gene" is a specific region on the genome that correlates to a specific inheritable trait (like eye color in humans: brown or blue). Not all areas on the gene contain inheritable material, some areas regulate the amount of expression of a certain trait. DNA is made up of four bases: G, A, T, and C. (Remember the movie: "Gattaca"? That's where they got the name.) A is always paired with T, and C is always paired with G.

So, thinking of it like a book: the bases are the letters; the letters form words (ATG, ATT, CGC...); the words form sentences ("CTA AGA CAT CGC"); and the sentences make up the book. Only here the sentences make a gene, and the book is the genome.

[I found this after the fact: A basic reference to "What is Genetics": http://learn.genetics.utah.edu/units/basics/tour/ ]

 

So, theoretically, everything is all neatly planned out based on the combination of genetics from both parents. In theory, it's all competely predictable...

...but things don't always go according to plan. And that's when you have mutations. I guess this would be what you asked about Mother Nature stirring the mix. Mutations can be helpful, harmful, or neutral, but they broaden genetic diversity either way.

A harmful mutation would be something that kills the offspring before it's even born (or does not allow it to survive thereafter) -- it can also be something that makes survival harder for the organism, like albinos in the wild. Some do survive, but they generally don't thrive. A neutral mutation wouldn't cause much notable effect either way, and a beneficial mutation allows an organism to be especially good at doing... something that it needs to do in order to survive and reproduce.

An interesting mutation in dogs has been seen in whippets, producing what is called a "bully whippet." This mutation affects a protein in the body that regulates muscle growth. "A 2007 study identified a myostatin mutation particular to whippets that is significantly associated with their athletic performance. Whippets with a single copy of this mutation are generally very fast; those with two copies have disproportionately large musculature and are known as 'bully whippets'." [source] (It can also appear in bovines, sheep, mice, and once in a human.)

This is Wendy. She's a bully whippet, but she's not the only one in the world. Her parents were racing champions. A single copy of this mutation is excellent for racing whippets. Two copies... ehm... not so much

[source and Info -- pic1]

[


CaptMike

by CaptMike on 06 February 2008 - 15:02


Many authors of the myostatin studies have speculated that interfering with the activity of myostatin in humans may reverse muscle wasting disease associated with muscular dystrophy, AIDS and cancer. Some predict that manipulation of this gene could produce heavily muscled food animals. Indeed, current research is underway to investigate and develop these potentialities. Sure enough, a large pharmaceutical company has recently applied for a patent on an antibody vaccination for the myostatin protein.

A medical doctor and author of weight training articles asserts that overexpression of myostatin is to blame for weight lifters that have trouble gaining muscle mass. The spokesperson for a supplement and testing lab erroneously implied that the "rarest" form of mutation in the myostatin gene is responsible for a top competitive bodybuilder's massive muscle gains, not taking into account the performance-enhancement substances the bodybuilder may be using. The public media has, of course, predicted that "steroid-popping" athletes will take advantage of myostatin inhibitors to gain competitive edge (3).

Many of these assertions are unfounded or they misrepresent the science. Granted, the possibility exists that manipulation of the myostatin gene in humans may be a key to reversing muscle-wasting conditions. However, too little is still yet unknown regarding myostatin's role in muscle growth regulation. It is imperative that research demonstrates that the loss of myostatin activity in adults can cause muscle tissue growth. Likewise, research must also prove that overexpression or administration of myostatin causes loss of muscle mass. Also important is to know if manipulation of myostatin will interfere with other growth systems, especially in other tissues, and result in abnormal pathologies. Although McPherron's gene knockout mice did not experience any other gross abnormalities, mice are not humans.

 


CaptMike

by CaptMike on 06 February 2008 - 16:02

We do not fully understand the roles of myostatin in exercise-induced muscle hypertrophy or regeneration following muscle injury. Until we do, it may be premature to blame the lack of hypertrophy in weightlifters on overexpression of myostatin. Nor does the research support the claim that a top bodybuilder's muscle mass gains are resultant of a detected mutation in the myostatin gene. The research simply does not advocate blaming genetic myostatin variations as a source of significant differences in human phenotypes.

Considering the history of the athlete's propensity, in the public eye, to abuse performance-enhancement substances, the media's prediction of myostatin-inhibitor may or may not be warranted. We all know that today's athletic arena demands gaining the competitive edge to maintain top level competition. For many athletes, that is accomplished by supplementing hard training with substances that enhance growth or performance. Whether or not myostatin inhibitors will be added to the arsenal of substances is difficult to predict. Until science reveals the full nature of this growth factor and its role in the complex regulation of muscle tissue, and researchers determine its therapeutic implications, we can only surmise. Despite attempts to tightly control any pharmaceutical uses of myostatin protein manipulation, they will likely surface at some point in the black market world of bodybuilding supplements. Let us hope that science has determined the side effects and the benefits by that point

http://www.ctv.ca/servlet/ArticleNews/story/CTVNews/20070530/strong_toddler_070530/20070530?hub=Healthhttp://www.musclephotos.com/myogene.html

 

 


CaptMike

by CaptMike on 06 February 2008 - 16:02






 


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