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Post by Deleted on Dec 8, 2012 10:29:29 GMT -6
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Post by nicky on Dec 8, 2012 12:35:07 GMT -6
I agree. I was looking through all the dilutors and saw this again. |
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Post by bookcliff on Dec 8, 2012 13:25:17 GMT -6
glad you brought that up, I've wondered about that ever since it was posted. Have always thought that something like this example might happen (it it isn't a typo and don't get me started right now on the Assn dna kit/tests/reporting after this week)
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Post by jbeever on Dec 10, 2012 9:23:52 GMT -6
In regard to the difference on how Charolais smokies and Simmi greys are treated at the sale barn, yes this may have something to do with the occurrence of rat-tail more often in the Simmi cross than the Charolais. The occurrence of rat-tail has more to do with the interaction with other pigmentation genes. The best data currently available suggests that rat-tail will occur with any dilution allele where white pigmentation is present in the tail switch.
This data was presented by a group in New Zealand where the use of Hereford bulls on Holstein cows is fairly common for non-replacement calf production. A great deal of these calves have rat-tail which was initially confused with hypotrichosis in these cattle.
In today's "less spotted" cattle the presence of rat-tail is significantly reduced in even Simmi cross cattle.
As an add-on to the discounting of these cattle, Cundiff and colleagues published a paper providing strong evidence that rat-tail cattle performed the same as contemporaries back when this was a bigger problem, i.e., when French Simmi was in heavy use.
Funny, attitude toward them never changed.
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Post by Deleted on Dec 10, 2012 9:49:09 GMT -6
In regard to the difference on how Charolais smokies and Simmi greys are treated at the sale barn, yes this may have something to do with the occurrence of rat-tail more often in the Simmi cross than the Charolais. The occurrence of rat-tail has more to do with the interaction with other pigmentation genes. The best data currently available suggests that rat-tail will occur with any dilution allele where white pigmentation is present in the tail switch. This data was presented by a group in New Zealand where the use of Hereford bulls on Holstein cows is fairly common for non-replacement calf production. A great deal of these calves have rat-tail which was initially confused with hypotrichosis in these cattle. In today's "less spotted" cattle the presence of rat-tail is significantly reduced in even Simmi cross cattle. As an add-on to the discounting of these cattle, Cundiff and colleagues published a paper providing strong evidence that rat-tail cattle performed the same as contemporaries back when this was a bigger problem, i.e., when French Simmi was in heavy use. Funny, attitude toward them never changed. its a funny deal to be on the wrong side of perception.... something hereford knows all too well. |
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Post by jbeever on Dec 10, 2012 12:13:10 GMT -6
Firstly, again, my comments were not directed at anybody in particular but based on my experiences within the livestock industries, not simply the beef industry and not just Herefords. We have solved lots of problems in several species thus, I have communicated with hundreds if not thousands of breeders. The issues that I describe are by far the ones that I have to address, and as I indicated, most often opinions remained unchanged. My guess is that yours will remain unchanged also regarding the origin of IE, but who's to say.
The proof we have regarding IE is based on the way that mutations happen over time. I'll use the NH mutation in Angus to help explain. Mutations happen at a single point in time, in a specific individual, on a specific chromosome. Mutation is a mechanism of generating genetic diversity. So, for instance, I can tell you that the NH mutation occurred in Precision 1680 and occurred on the chromosome that he inherited from his father, Bando 155. The reason I can say this is that when a mutation occurs, it is in the "context" of all the other genetic variants (mutations) that are present on that chromosome.
So, by looking at the DNA variation all along the chromosome, by using things like SNP markers, I can see that the chromosome that had the NH mutation was exactly the same as the one present in Bando 155, minus the mutation of course. The non-random association of the mutant allele with alleles at the other markers, etc... is called linkage disequilibrium (LD). Because of LD, the mutation and other markers will be inherited together as a unit until LD is not present, called linkage equilibrium.
The rate at which LD decays is dependent on the distance the other markers are from the new mutation. Markers that are far away on the same chromosome will reach equilibrium within 1-2 generations due to recombination of genetic material during gamete formation. However, markers in close proximity to the mutation will take a very long time to reach equilibrium.
Using this kind of information, certain things can be concluded about mutations including their age and where they came from. For instance, the HY mutation in Herefords is only surrounded by about 250,000 bp from the original chromosome it occurred on, everything further away has reached equilibrium. Thus, I can conclude that this mutation is very old as compared to the IE mutation that is still surrounded by about 3 million base pairs. This would be consistent with what we know about the mutations also in that there is anecdotal evidence that HY may have been seen in the 50s, perhaps before, and the first IE calf was seen circa ~1993.
So, as to the evidence that the IE mutation occurred in Miles City germplasm, if we examine the region of LD around the IE mutation, what we can define is something called a "molecular signature" that is composed of a unique set of polymorphisms along the chromosome in that region. To determine where the origin of the mutation might have occurred, we can look for that same signature in the current population. In the case of IE, the single population with the absolute highest frequency (no other population is close) of that signature is the Miles City population. In fact, this turned out to cause us tremendous issues in determining where the mutation might have been.
As the Miles City herd has a very high frequency and its germplasm is continually introduced into the population at large, what we detected was an increased number of cattle that were homozygous for an extended chromosomal region that were not affected with IE, they all had L1 (Miles City) ancestors close in their pedigree.
Because of LD, we can usually, with a fair degree of accuracy, predict the genotype of an individual before actually knowing mutation by using all the closely linked markers. This was impossible with station-bred cattle until we knew the mutation as almost all of them had at least one copy of the chromosomal segment that the mutation occurred on. For cattle that had no L1 germplasm in the first several generations of their pedigree, we could predict genotype quite readily almost a year before we found the mutation.
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Post by Deleted on Dec 10, 2012 17:59:55 GMT -6
"This was impossible with station-bred cattle until we knew the mutation as almost all of them had at least one copy of the chromosomal segment that the mutation occurred on. "
Couldn't the mutation have occured in a non Miles City animal that inherited the "chromosonal segment" from its ancestors that were common ancestors to the foundation cattle at Miles City?
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Post by jbeever on Dec 10, 2012 20:00:34 GMT -6
Although not impossible, I'm going to say no for two reasons. The problem is that the question is pretty open-ended in that any chromosome that the mutation occured on would have been in the foundation stock. Thus, the answer is based on the timing of actually calling the line, L1.
Firstly, based on the rate of LD decay (which is predictable based on distance) and size of the region still in LD around the mutation, and estimating the number of generations based on this information, the L1 cattle would have been well established and closed by that time, probably early 70s.
Secondly, if that were the case, there would have been lots of carriers in the Miles City herd; in 2008 there were none. In order for this to happen, the mutation either happened in an animal outside the Miles City herd within a generation or so, or because of the selection scheme at Miles City, the mutation was present on the station, but was eliminated by random drift.
Let's say the original mutation happened in a cow, she would have limited opportunity to leave offspring over her lifetime and only half of them would have had the mutation. So for the first couple generations the number of animals that have the mutation remains very low. In cattle populations where natural mating is the norm, it really only increases in frequency when it winds up in bull. AI can really contribute to increasing the frequency in a single generation.
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Post by George on Dec 10, 2012 20:22:27 GMT -6
Dr. Beever, are you comfortable in discussing exactly which Hereford that the mutation that causes IE occurred?
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Post by rockmillsherefords on Dec 10, 2012 20:57:59 GMT -6
I don't need to press the "purity" button again, but the white-face trait is controlled by a different locus in Herefords and Simmental. We have some good ideas on what the gene in Herefords is, but it is not so clear in Simmental. If we had a DNA test for both, makes you wonder how many other lines of cattle that the "purists" in the crowd would have do get rid of because they have gone undetected until now and considered pure Hereford because they are registered. AHA paying you NOT to work on that particular dna test I reckon.  |
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Post by jbeever on Dec 10, 2012 21:35:08 GMT -6
Yes, the only factual information is that progeny data indicate for sure that HH Advance P242 was an obligate carrier.
If I were to speculate, I would suggest that 883 and A482 on the bottom side of his pedigree couldn't have been carriers because they each sired enough progeny that by now we would have detected another "pedigree path" back to them without going through P242. That leaves maternal transmission only on the bottom side that might go as far back as 2-3 more generations.
On the top side, its hard to say. None of those had enough progeny to tell anything, L392 only had 4 sons that went on to produce more than 10 progeny including P242.
So, either it occurred in P242 or within 2 generations behind him. Not that it is very important, but archiving DNA on inidividuals is pretty handy for figuring these things out. In the case of AM and NH in Angus, we got access to a frozen cell line on Precision's dam that was saved from cloning.
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Post by George on Dec 10, 2012 21:44:05 GMT -6
Yes, the only factual information is that progeny data indicate for sure that HH Advance P242 was an obligate carrier. If I were to speculate, I would suggest that 883 and A482 on the bottom side of his pedigree couldn't have been carriers because they each sired enough progeny that by now we would have detected another "pedigree path" back to them without going through P242. That leaves maternal transmission only on the bottom side that might go as far back as 2-3 more generations. On the top side, its hard to say. None of those had enough progeny to tell anything, L392 only had 4 sons that went on to produce more than 10 progeny including P242. So, either it occurred in P242 or within 2 generations behind him. Not that it is very important, but archiving DNA on inidividuals is pretty handy for figuring these things out. In the case of AM and NH in Angus, we got access to a frozen cell line on Precision's dam that was saved from cloning. Thanks. From my quickly reading through what you've written here, I was getting the impression that you thought that the "place" where the IE mutation occurred was inherited by P242 through his paternal grandsire. |
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Post by Deleted on Dec 15, 2012 21:02:40 GMT -6
Although not impossible, I'm going to say no for two reasons. The problem is that the question is pretty open-ended in that any chromosome that the mutation occured on would have been in the foundation stock. Thus, the answer is based on the timing of actually calling the line, L1. Firstly, based on the rate of LD decay (which is predictable based on distance) and size of the region still in LD around the mutation, and estimating the number of generations based on this information, the L1 cattle would have been well established and closed by that time, probably early 70s. Secondly, if that were the case, there would have been lots of carriers in the Miles City herd; in 2008 there were none. In order for this to happen, the mutation either happened in an animal outside the Miles City herd within a generation or so, or because of the selection scheme at Miles City, the mutation was present on the station, but was eliminated by random drift. Let's say the original mutation happened in a cow, she would have limited opportunity to leave offspring over her lifetime and only half of them would have had the mutation. So for the first couple generations the number of animals that have the mutation remains very low. In cattle populations where natural mating is the norm, it really only increases in frequency when it winds up in bull. AI can really contribute to increasing the frequency in a single generation. "Although not impossible, I'm going to say no for two reasons. The problem is that the question is pretty open-ended in that any chromosome that the mutation occured on would have been in the foundation stock. Thus, the answer is based on the timing of actually calling the line, L1." If you look at P242's pedigree and the two maternal great grand dams you point to as potential carriers you will see that they both descend from Mark Donald bred cows that were born in the 1950's. Since the Miles City Line 1 program herd was closed to outside blood in the 1940's, it appears to me that P242 descends from different foundation stock than the foundation stock used at Miles City for the Line 1 program. They may be closely related to the Miles City Line 1 foundation stock, but they are a different set of cows. |
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Post by strojanherefords on Sept 7, 2019 10:48:09 GMT -6
I can prove that HY and IE are uniquely Hereford. Fact is, mutations happen. The idea that genetic mutations can only enter a breed through some type of "contamination" is a super-myth that I spend way too much time explaining to people who's opinions would remain unchanged anyway. In the case of DL, its more difficult. The issue is this, because DL is not detectable in red-hided cattle, you cannot produce evidence to refute that DL may have existed in ancestral breeds that all red breeds were derived from. Thus, whether the presence of DL is something that has always been part of the breed is an open question. However, the fact that the frequency of DL carriers among old-type Simmental, Fleckvieh and Gelbvieh cattle is quite high and there was active "breed complementation" happening in the early 80s for all the British breeds provides strong suggestion that DL is a mutation that occurred closer to the geographic origin of those breeds and was introduced into Herefords. I don't need to press the "purity" button again, but the white-face trait is controlled by a different locus in Herefords and Simmental. We have some good ideas on what the gene in Herefords is, but it is not so clear in Simmental. If we had a DNA test for both, makes you wonder how many other lines of cattle that the "purists" in the crowd would have do get rid of because they have gone undetected until now and considered pure Hereford because they are registered. What is a fair reading of "I can prove that HY and IE are uniquely Hereford"? Does it mean that Dr. Beever has evidence that proves that IE and HY originated in the Hereford breed? Or is he saying that he has the ability to determine where the traits came from? |
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