E G Price Writings

The lone poster on other sites that doesn`t post here that I wish was a participant at KC...mk

I apologize up front for lack of brevity, I just do not know enough to make it short. It is an attempt to bridge many of the different posts on diverse topics while stimulating additional thought as to how our industry may compete more efficiently. I offer this as food for thought to the fishes as well as the sharks......Hmmmmmmm

Within Breed Heterosis?

Hybrid vigor-scientifically known as heterosis-is found throughout the cattle industry. Animals with diverse parents tend to be more vigorous and grow faster than those of within breed matings. “Why” remains the main question in many inquiring minds. It is not a simple issue requiring little thought and limited experience to really understand the process.

Making wide crosses requires that divergent types exist. The process of creating species and, to a lesser extent, breeds continues to be debated to seemingly no end. Inbreeding, line breeding, and mating of like phenotypes is certainly involved. Selection, whether natural or manmade, is also important. Specific DNA regulating the phenotypes is fixed by homozygosity or may be controlled by heterozygosity. Each method is effective for commercial manipulation and both must include homozygous types in the commercial generations.

One possible explanation may be visualized if one imagines 1,000 SNP on chromosomes other than X and Y from two breeds of cattle we choose to mate. Breed A cow is homozygous at 400 of these SNP and breed B bull is homozygous for 600 SNP while they have 300 of these SNP homozygous with identical DNA in common. That is to say that the cow has 100 SNP homozygous that are not found homozygous in the subject bull. The bull has 300 homozygous SNP not found homozygous in the cow. Thus, when mated, we can predict a shift in the DNA of the offspring to parental specific DNA at 400 SNP, some from the cow and some from the bull. Science seems to have no consensus as to how these benefit the animals growth and vigor. We know we will have no shift at 300 SNP homozygous in common to the mated pair, thus conserving genotype and probably phenotype found in both breeds. Because of random assortment from the heterozygous parent, there are 100 loci that will add SNP from the cow that were not homozygous in the bull. Approximately half those will be homozygous in the offspring and half will remain heterozygous as found in the bull. The effect of the more highly homozygous (inbred) bull from breed B will add approximately 150 new homozygous SNP in the offspring , these found heterozygous in the cow. Which is more important, the new homozygosity or lowered heterozygosity on the phenotype of the offspring? Understanding is difficult indeed for lack of experience or precedence. No genome company is reporting specific SNP at this time to individual breeders. Readily apparent are the greatly increased opportunities in the F2 offspring expanding new possible combinations, thus spreading the chance of new and different types. The bell curve is narrowed by backcrosses, linebreeding and selection for traits not influenced by heterosis.

When selecting based on performance measures, we get a mix of heterozygosity and homozygosity available among various offspring. It is reasonable that the faster growing, more vigorous animals among the offspring may be the ones with more heterozygous makeups, such as the cow when compared to the bull above. In variable environments, the heterozygous loci may confer an advantage by having two genetic responses within the diploid genome. This response has limited heritability because of variable DNA assorting to the offspring. The question remains until we know the exact makeup of each SNP and relate this back to the population. “On the average or single figure reporting” does not help eliminate variables in this rational endeavor to understand heterosis. Selection based on known SNP differences is practical, though dampened by genetic background effect. If reports are for homozygous loci only without consideration of favorable or unfavorable associations with phenotype, how does that help breeders selecting for traits favored by having both parental types DNA at specific loci? Does this help predict uniform desirable outcomes from matings?

Now imagine cow A and bull B types are within your own purebred herd (diversity is known to exist in DNA reports). Which offspring would you select based on numbers of uniform SNP data if available, those more homozygous or others more heterozygous in their DNA makeup? Does it matter if offspring are uniform because of predictable heterozygosity or uniform because of increased number of new loci with predicted homozygosity from the same type matings? Either way predictability demands uniform parental genomes in the final generations. Replacement and terminal cross matings predicted by selection of parental animals are essential for desired uniform results. Assortment by larger numbers of 1:2:1 loci found in F2 type segregation in offspring will not help predictable outcomes, but may add new, more broadly adapted types in the long run. Some true breeders identify objectives and select toward newly established goals while others conserve and maintain animals other breeders consider to be obsolete. Nature is providing both functions concurrently.
Breeds exist for many reasons, but most of them are natural. Many breeds are old, others only a few generations in existence. Selection for commercial traits is under close control of man, but capricious phenotypes are found naturally, their numbers only enhanced by intervention by mankind under domestication. Adaptation to natural and manmade environments requires that genetic variation be present in the population of breeding animals. The industry manipulates variation within and among breeds of cattle, yet contains many seemingly unselected specimens. The latter are not worthless as they serve as bad examples in today’s environment, yet these unselected types may also bring needed diversity in the future. We should celebrate the diversity for the generations of breeders who may demand different commercial and adaptive traits from domestic animals and also those breeders who develop uniformity within their purebred herds.


E.G.Price 2/2/2012

A few years ago I had the opportunity to meet Glen in Denver. I hope he will come over and share some of his knowledge and background.

Keystone wrote:

A few years ago I had the opportunity to meet Glen in Denver. I hope he will come over and share some of his knowledge and background.

his advantage email doesn`t work; I suppose you should call him Kent

I need to do that Mike.

E G has made contact; now I better read the above instead of skim ...I rarely run across anything that deserves more than a skim...heck, the above might even take some study

Well I made it through the registration process, Mike and Kent. Maybe I, too, should read instead of skim! Thanks for the invite. As you know, Some of the tools we were using in our program made sense to us, but apparently not to all. That's the way we should like it, except we based our program on technology that moved out from under us in one generation of Bio-companies. They reproduce faster than cattle, so here we are orphaned and seeking other tools. Oh, well, the technology was planned to be obsolete anyway.

welcome E G,
I am attracted to any writing I can`t dispel with a one-liner; ...I hope I studied your above piece enough to not make a complete fool of myself, but then again, we do that on purpose here a lot, and laugh doing it...
but seriously, starting at the last first...

We should celebrate the diversity for the generations of breeders who may demand different commercial and adaptive traits from domestic animals and also those breeders who develop uniformity within their purebred herds.

are you saying that we should celebrate the random diversity created by varied breeder goals, or the diversity that nature clings to as some try to breed types with less variation?

is everything we do all right?
singing

It's all right, have a good time
'Cause it's all right, whoa, it's all right
Now everybody clap your hands
Give yourself a chance
You got soul, and everybody knows
That it's all right, whoa, it's all right ?

I am reminded of the TV ad that says feed it to Mikey, Mikey will eat anything. Well, I see that was not Keeney in that ad. That diversity statement was meant to say we are in an ever changing environment, so we need some diversity to adapt our populations for perfect fitness. None of us attain perfect fitness, none of us has the magic goal, but many approach commercially adequate fitness in our herds. Fads cause swings in the selection pressure applied to the national herd. Genetic types shift. Many breeders succeed because of the change and, in fact, direct the moving standard to favor their operations. Ads and marketing. Others conserve their biological type and let the pendulum of demand swing, safe in the knowledge they are better adapted to natural events than the competition. Insurance for the future is found in both types of herds because of the variation and uniformity at the same time. If everybody is thinking alike, noone is really thinking. All your eggs in one basket. The kind of things our parents taught us.

G nome wrote:

I am reminded of the TV ad that says feed it to Mikey, Mikey will eat anything. Well, I see that was not Keeney in that ad. That diversity statement was meant to say we are in an ever changing environment, so we need some diversity to adapt our populations for perfect fitness. None of us attain perfect fitness, none of us has the magic goal, but many approach commercially adequate fitness in our herds. Fads cause swings in the selection pressure applied to the national herd. Genetic types shift. Many breeders succeed because of the change and, in fact, direct the moving standard to favor their operations. Ads and marketing. Others conserve their biological type and let the pendulum of demand swing, safe in the knowledge they are better adapted to natural events than the competition. Insurance for the future is found in both types of herds because of the variation and uniformity at the same time. If everybody is thinking alike, noone is really thinking. All your eggs in one basket. The kind of things our parents taught us.

agreed EG; and the differences of genetic direction will often be more because of human nature than environmental or market need; accept and let it be...
so on to heterosis and more...my first question is a leading one, and I am not divulging the second because if the first is too foolish/dumb etc, I don`t want to be foolish twice in a row I am dealing with a plant breeder here; not a "put the boys with the cows and make the babies" concept; right Bob H?

Why doesn`t the 50k test for Angus work equally as well for Hereford?

Maybe I should pass on this one....but I won't. You got me to thinkin' again . We would predict that a test based on SNP from one beef breed will not mark the genome as well on cattle less related. However, the routine of checking for markers does include interprettion. Genetic background may change phenotypic expression. Complimentary genes in the offspringof one breed may be masked by genes fixed in the process of linebreeding in another? The phenotypic response may have been attributed to a marker that is not present at all in the Hereford genome. To me, that simply says the cattle are not genetically identical. We would expect the same to be true within the Angus breed, but then we call one SNP variant favorable and another unfavorable assume big chunks of DNA are similar allowing for the 50K judgement to occur. There can be mistakes within the breed. An F1 cross might be of use in the causal reason(s), an F2 group would add resolution to any findings in the F1. Backcrosses to either parent line would also help. Even within a breed, we may be mating for most unrelated animals in growth trait measures.

Since I seemed to escape being terribly foolish on question one even though I can only feel comfortable with layman or less terms; I will attempt the followup question...might the fact that the contributing sequences, markers, snps, or whatever term is correct...that are responsile for the same phenotypic trait expression {let`s say growth} is located in different places in different breeds, contribute to heterosis between breeds? or does difference all along the chain create the greatest heterosis effect? the ole big A, little a as I learned things...
As DV tells me from time to time; just pounce on me if you need to, I can take it

Nice follow up question that actually was the purpose of the first postings you brought from outside Kenney's Corner. I would offer the following follow up on your first question which may help us in finding answers. In the early stages of beef genome analysis by SNPs(single neucleotide polymorphisms), several were found associated with tenderness in tested animals. Two types of enzymes were found, one controlled the fate of calcium in cells of animals after death, and the other controlled the first enzyme by blocking it somehow. Among these markers was one that clearly marked favorable tenderness in Angus but when found in Brahman crosses, it was difficult to coorelate. That marker (I forget the exact SNP ID) was pulled from the panel of one company and it failed third party certification because it was not accurate. It is considered that the particular marker was not a part of the causal gene actually coding for the enzyme protein for tenderness and that a crossover had occurred between the marker and the genesequence during the process of diverging into breeds. Brahman and British breeds diverged many generations ago. This process of crossover actually is a strong criticism of markers that are not actually a part of the active gene. It does little good to select based on markers when they are 50% accurate. Basically, in Brahman cattle, the same SNP marker was associated with a less favorable gene type for tenderness. This did more harm than good, so the SNP was abandoned by the company.
Today, SNP are used in many different ways, chosen randomly along the chromosome and then lined up like soldiers to be analyzed. If the line is continuous as in parental forms, it is interpreted that no crossover has occurred. Still, someone has to do the complete DNA profile and associate it with things we can measure in the phenotype, listing the linear neucleotide pairs of the gene at some point. Note that SNP technology has changed continuously from a few to 50 thousand in about 10 years. Ranchers cannot direct much change in 5 generations within his herd. Selection based on SNP data speeded the selection process, but some of it was in the wrong direction. But reporting averages does little more than poorly associated SNP markers did.

Now about the second question...As we know little about growth inheritence, except with dwarfism, etc, it seems we will have a difficult time trying to say a single gene controls it. We know that ain't so most of the time. Multiple genes are involved, and whether they are all on one strand of DNA or on both may not be as important as that they are in the cell and switched on at the proper time to favor growth. If they have been rearranged, they may in fact be present by silenced or complicate other biological processes by being swithced on out of sequence. I do not know the answer, but asking the question is important to us all. Thanks, Mike.

aww yes, so Bob`s daughters theory finally takes precedent once again...there comes a time when we quit analyzing, accept some inadequacies, and turn the boys with the girls and make some new babies
then in the winter, we can try and figure out what happened...why does a coin land about half the time heads, half the time tails, if we toss it enough? could it be it has two sides? ...what if both sides were heads?...

Mike, I always wonder about those rare times when the coin lands on edge, but I have been in games where the double headed type must surely have been used by my opponents.

Dennis Voss wrote:

EG here is one of those times that the coin landed on its edge.

E G,
Will watermelons and cucumbers cross pollinate ...and produce seeded fruit ?

Squash and cucumbers will, along with peppers and okra. It make an edible product in the latter, the first ain't fit to eat. I doubt any of them would reproduce and that is about the extent of my knowledge on genomes, genetics, and square roots.



Bootheel, not much use today

Mike, I have little experience with attempts in cross pollination of cucurbit species. However, I once had a cucumber trial next to a seedless watermelon procuction field in which triploid and diploid watermelons grew. Those cucumbers set the best crop I have ever seen in cucumbers, I knew that the cucumbers were partially parthenocarpic (set without pollen), but these had a cucumber at every node on the vine and they were large. I have to credit N. Carolina State for the trial cucumbers. I never developed any commercial varieties of them, I always figure I missed a great opportunity to do so.

the first ain't fit to eat
does that really matter Joe, so long as it grows big and fast ?

"... you can live on it, but it tastes like shit." Mick Dundee

Mike, back to the original copy here----A follow up post on another site was in response to assumptions. Some may have read it, but I paste that response here to continue my thought pattern that within breed vigor is no more than a continuum of DNA variability and its impact on the animals subject to environmental variation we find between breeds.

Knabe, I am looking for answers, not prejudging or assuming for the most part. I find it interesting that the average offspring from the example mating above has more homozygous loci than either parent, actually 650 predicted! This is possible because the mating included 300 in common, thus conserving these while the rest of the combinations maintain or add new ones at loci in which one parent is homozygous and the other heterozygous. I also find it interesting that the more homozygous parent (bull) adds 150 new homozygous loci and the cow likewise adds 50. The loci with heterozygous condition as found in both parents adds another 150 homozyous.

The common figure of "X" number of loci heterozygous is probably less important than the new homozygous ones created by the combination. Many previously heterozygous loci are now homozygous. The picture is complicated and we didn't even mention gene action, switches, lethals, meiotic drive, linkages, etc. I only considered the numbers of known SNP loci that have either ++ or -- present as opposed to +-or -+ for the known variant base pairs. Your idea posted earlier of 0,1 or 2 reporting of "favorables" might have value, but until we know their location on the genome and have parental documents as well, little can be gained.

Even though there is no provision of gene action here (dominant or recessives associated with the SNP), inheritance patterns can readily be seen to favor the cow or the bull depending on those DNA sections that are more homozygous. Line breeding can be reflected in these sections. To test those, we need the read outs of each major chunk of DNA. Performance measures grade these according to natural and our own artificial standards. My questions, that science has thus far failed to answer to my satisfaction are these: Is the reduction in vigor with extreme line breeding caused by the decrease in heterozygous loci or due to homozygous deleterious ones not offset by a good one? Can we select for major chunks of DNA that are associated with good traits by selecting those that do not recombine in miosis or during reunion of gametes in the fertilized egg. Of course that is the stuff behind the IP curtain we are each expected to pay for as breders and owners of animals while not getting the necessary data until it is locked up and more fees paid direct.