genetic diversity

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knabe

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http://www.abcnews.go.com/Health/Story?id=3275245&page=1

decent article alluding to the fact that a lot of diversity is selectable other than just the 25,000 or so genes.

though i have no experience breeding cattle, i can't help thinking that there is some diversity worthy in PHAC animals, particularly the fullbloods, as this defect represents only 1 base pair of diversity out of over 2 billion.  the test allows us with almost certitude to cull appropriate animals (assuming there are no alternative alleles).  as it stands now we are going to cull them all, rather than allow any to eliminate the one base pair, and further distill the gene pool. it is sad we will not be able to visit those combinations again, albeit one base pair changed.

the comment "We are far, far more similar to each other than we are different."  is misleading.  i still need a mirror to see myself.
 

Telos

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Knabe, your thoughts and article on this is really intriguing. Looking through a lot of Maine pedigrees, it's interesting to see how many modern day pedigrees of which are PHAF had a carrier or two and sometimes many more in their ancestry. I feel, with the test, breeders can really utilize PHAF cattle which come from carriers. Dr. Beever's test is perhaps the salvation of a great breed of cattle. Taking full advantage of it, I strongly feel, will prove beneficial for contributing to the continued improvement of the breed.

Knabe, my question is, why do the carriers in many cases appear to be better? It is not just a coincidence to have ten or more A. I. carrier sires coming from one herd and only a few PHAF. Was the selection pressure put on something regarding phenotype of which the breeder recognized? Do other genes travel together along with this defective gene? Sorry for my ignorance about genetics, but it is to abstract for my poor brain to comprehend.








 

knabe

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i can't say why, but only speculate.  Barrelracer and Dr. Beever obviously have the most insight as they know the gene and a particular pathway that may be involved.  since the phenotype supposedly is caused by a single polymorhism (there are 4 letters in the genetic code, GATC) one base pair has been substituted for another, i don't think there is any linkage of genes going on, though i can think of a couple scenario's where that could happen.  in the past, they have mentioned somewhere that it wasn't a gene that they thought of.  this is often the case as people go gene hunting.  over and over, it's not what we thought.

the pathway involved is probably more likely.  for instance, and i know, this is going to sound ridiculous, but in a fish called stickleback, there is a gene responsible for the elimination or reduction of the hip, or pelvis, along with 4 other genes. it is related to pelvic reduction in other species, notably manatee's.  perhaps it will be a gene like this, except that the carriers are the ones that have the pelvic increase phenotype.  i would like to see a lot of washed cattle standing side by side with their status on a card above them and go over these animals with those who selected the carriers. perhaps the structure has more evenly laid down calcium, perhaps some subtle clues they were looking for that when the animal was static, it really stuck out for them, and is different when they walk, or is the same, who knows, but they do.  i wish there was an environment where all this could be open.

perhaps the PHAF ones just required more numbers to get great ones and right combo of genes than the carrier pool due to the combination of genes and PHA lowered the threshold of the right combo because it was affecting a pathway with fewer/more genes, who knows.

http://www.jstor.org/view/00143820/di000328/00p0195o/0
http://www.nature.com/nature/journal/v428/n6984/full/nature02415.html

in cattle, something the opposite could be happening, but that it's related to genes that seem to combine, and in the presence of a heterozygote state of the PHA gene, they really look the bomb.  it is my stupid uninformed opinion that there are more than just the two groups of cattle that are selectable than the PHAF and PHAC.  i don't have anywhere near the eye to pick out what was selected for, but that we will eventually be able to figure out these groups which may account for the unpredicability of phenotype with being a carrier or free.  from a fullblood perspective, i see this as an opportunity not to throw out indivduals if they have merit in another trait of interest unrelated to a look, but another pathway such as marbling, extended ability to lay down marbling independent of photoperiod, independent of high grain feed.  i think it is a shame to lock out those genetics, if we now have a test, granted it will take more time and money, but at least you don't have to do a test cross anymore for PHA.  I feel this is huge.

so, if in the heterozygous state, PHAC, gene regulation is thrown off a little, and in the presence of the right combination of genes and copy number, perhaps a phenotype is visible to the people who have been selecting these.  perhaps the androgenous females is another phenotype that is created by an "unoptimzed" pathway.  i know people have stated over and over DL, etc, that one's they thought might be carriers according to phenotype were not and vice versa.  perhaps that's because the individual didn't have the right combination of genes.  perhaps there is a linkage to the genes in the pathway affected and a crossover hot spot somewhere, even in line with the PHA gene that is causing some of the unpredictability to the eye.  this is why i would really like to see a few breeders opinion on this that generated many of the carriers and what they saw.  years ago, breeders were not scared of linebreeding.  they knew there would be bad as well as good genes, and this was the quickest method to distill a product that had a high degree of potency.  the push to the mongrelization of the entire us cowherd will not allow this, and always is proved by the fact that  time after time, along comes someone who is not motivated by a high turnover of bankers money, and they will linebreed and everything will change again.  it's another figure 8 going on.


This is why i am so interested in line breeding in general and maine's in particular.  maine's have had very little linebreeding, perhaps due to their carrying more genetic defects at their current stage of utility than other breeds today, but not necessarily the case before other breeds were started.  as others have mentioned before, most breeds are simply land races of selection to excel on the environment they were in.  color patterns, sweat glands, horns, etc were the easy markers that distinguished them.  however, others included the ability to be dual purpose, excel at marbling on grass.  in the past, cattle were fattened to a much more mature age, and those that excelled at this were fixed as a phenotype.  economic forces played a role as poor farmers couldn't feed their cattle for 3-5 years and needed fat beef with less resources, similar to the corn thing going on now.  people took the fat off the outside of the carcass of holsteins and put it on the inside, all the while breeders thought they were getting rid of useless fat.  maines' seem to have a lot of diversity and opportunity to fix genotypes to various environments, but probably not like mine where the grass is mostly annuals and dries up fast.  this is also why i am interested in high sugar forages which have high water soluble carbohydrates.  i actually think the lines which are not fixed offer some opportunity for progress.  i think maine's have an advantage over other breeds by not having to shortcut the process as other breeds have by infusing other breeds, such as the one's we all know have.

one final comment, and red, correct me if i'm wrong, but telos has gone more circles with his post with less words than i ever do.  i feel humiliated.  ;D

on one hand you say good ones have carriers in the background, then you say there is more good ones who are carriers.  this could be at least two things.  the noncarriers were not accounted for just as the homozygous dead one's werent either, or the combo of cow and bull's genes only recombined for whatever reason, perhaps not due to chance alone to have more carriers, and not a 50/50 distribution.

and finally, genes travel together until a crossover point, then they get the genes from the other parent on the same arm, then back and forth.  this is recombination different than just using  different parents.  this is a whole can of worms, because some species have whole chromosmal rearrangements to foster diversity becuase for whatever reason, they don't have access to a lot of mating opportunities.  some frogs are this way, poplar trees, organisms which have lots of babies, coral for example.  oh genetics is fun.

and really finally, there is only about 10 people who can answer this question "why do the carriers in many cases appear to be better?"  perhaps they are not, they just look better (other than they are a carrier).  none of the above is really probably helpful.
 

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