PHA hot off the presses!

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cowz

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DL,

You deserve a hand for all of the time you have spent educating us on these boards!  Thanks!! (clapping)

You know me, I wont go away with out asking an odd question.  Since it is apparent that there could be  2  types of PHA, different breeds,  is it possible that in time a PHA mutation could occur within any breed?  I remember the hydrocephalus days in Herefords and Angus.  I know that is probably a stretch, but wasn't alot of that problem a result of the intense linebreeding (inbreeding) going on in that era. 

Just random thoughts.  This whole topic is totally fascinating.  And scary.  Hope you dont have to put coats on calves this week!
 

knabe

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linebreeding creates what is known as near isogenic lines.  this means that after as little as 6 generations, offspring are homozygous for most traits on both chromosomes.  if there is a genetice defect which manifests itself in the homozygous state, they will show up.  in the old days, the defects disappeared in the ditch and the low performers were eliminated from the pool as well.  if one took two near isogenic lines from two different breeds of cattle, and crossed them, theorhetically there would be more hyrbid vigor than between breeds without line breeding, although not always the case.  the difference between the process in plants and animals, is that in corn, the inbred lines don't have to perform at all, and in fact are typically very poor performers.  this is not really accurate, but one could take a lowliner angus and cross it with a lowliner hereford (not a real breed, but not the dwarves either) and the offsrping would be a double muscled frame 8 steer at 16 months.

it is possible that mutations occur more frequently in the PHA and TH genes for whatever reason, and that other breeds have it, it's just that the popular lines don't have it.  if one did, look out.  just like maine's.  linebreeding of PHA really underscores how easy it is to uncover these defective genes and how hard it is to get rid of them if they are in popular lines.  in the old days, we didn't have genetic tests, we just had, well, ........
 

cowz

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(welcome)  Welcome knabe and Barrel Racer!

Wow, I am truly grateful that you are bringing your knowledge to our board.  Where were you guys when I was studying Genetics?  (When dinosaurs roamed the earth?)

I am positive that this group will come up with some great questions and further discussions on genetics.  Sometimes we all need a little time to ponder.  I know I only think of the good questions when driving, in the shower or at 3 am!!

Again, welcome! Glad to have ya!
 

garybob

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TH was first discovered in Galloways. Now it's Shorthorns' problem. Who cares where it came from. Let's get rid of it. Put the carriers between two seeded buns. It ain't rocket science. Remember Gregor Mendel said genes assort at random and Robert Bakewell said Like Begets Like.
 

AAOK

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DL said:
.

AAOK - We didn't have to test Draft Pick to know he is a carrier but apparently he isn't listed because there were no official results as of yet! Life is certainly strange, eh! DL (cow)

Strange, Yeh.  I'm glad I asked.  I have been wondering about that from the beginning of the carrier bulls being posted.
 

DL

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Great stuff eh!

garybob - if I recall correctly the Galloways aggressively determined carriers (by pregnancy termination, remember this was in the dark ages - the 70's) and they were not used. And while I agree with you 100% that not using carrier bulls will help to rapidly eliminate both defects, our situation today is complicated by the club calf, show cattle, get the great one at any cost. Humans have created these issues - now we need to deal with them. Al least (thanks to Dr B, Barrel Racer and let us not forget goodegg) have a test to help us make reasonable breeding decisions.

cowz - like knabe said with line breeding you are more likely to see these evil recessive traits rear their ugly heads! And I believe the potential for a spontaneous mutation exists at any time - good grief I could be mutating as we speak!

There is also an interesting "new" defect described in Angus cattle called Fawn Calf Syndrome - it has apparently been pretty well described in Australia and it is believed that some of the carriers of the defective gene originated from the US. I have a little handout I was sent about it if anyone wants it - nothing published yet. And by the way if you asked me to send you something and you don't have it - please ask again....

there is a syndrome in the cold windy snowy weather called foggy brain - it may be a combination of genetic and environmental - but it is sporadic - I am in the throws of it now!  (cow) (cow) (cow) DL

 

red

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garybob said:
TH was first discovered in Galloways. Now it's Shorthorns' problem. Who cares where it came from. Let's get rid of it. Put the carriers between two seeded buns. It ain't rocket science. Remember Gregor Mendel said genes assort at random and Robert Bakewell said Like Begets Like.

Gary Bob the trouble w/ thinking it's a Shorthorn problem came & bit me in the butt. I (when I was naive) bred a Warhorse cow to Cherry Bomb, never dreaming that I, a Maine breeder, could have problems. Bam, a TH calf, broke my heart. That educated me quickly that it wasn't a shorthorn problem but a cattle problem across the board. that is why we appreciate the work these guys in the labs & fields have done.
Red
And yes, I still have her, I'm just testing her calves & doing w/ them accordingly.
 

DL

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red said:
garybob said:
TH was first discovered in Galloways. Now it's Shorthorns' problem. Who cares where it came from. Let's get rid of it. Put the carriers between two seeded buns. It ain't rocket science. Remember Gregor Mendel said genes assort at random and Robert Bakewell said Like Begets Like.

Gary Bob the trouble w/ thinking it's a Shorthorn problem came & bit me in the butt. I (when I was naive) bred a Warhorse cow to Cherry Bomb, never dreaming that I, a Maine breeder, could have problems. Bam, a TH calf, broke my heart. That educated me quickly that it wasn't a shorthorn problem but a cattle problem across the board. that is why we appreciate the work these guys in the labs & fields have done.
Red
And yes, I still have her, I'm just testing her calves & doing w/ them accordingly.

I think one of the big issues is denial +/- ignorance +/- lack of education or understanding +/- misconception  - some people think that if the cow is only a little bit Shorthorn or Maine she can't be a carrier because she doesn't have enough in her to make her a carrier (remember it is just one gene - that is all you need!). Sometimes you go back into the pedigree of composite animals and find generations back an unnamed MA or Shortie - the better we are educated and the better we educate buyers and youth the better for the bovine! Ilook at it as a medical issue - bad gene lets make it go away - others are willing to live with the risk of creating carriers or affected animals. I am not. Is anyone surprised??? (cow) (cow) (cow)
 

cert

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red said:
I know I went into major depression when I found out the my Gold Club heifer tested positive for PHA. She was going to be a donor cow but nixed that idea fast.

Red (cow) (clapping)

Red I have to aplaud you on your decision to not flush the Gold Club heifer. I know that must be hard on your operation but it deserves a pat on the back at the very least. We need more folk like you in the industry. Then TH and PHA would not be as big of an issue.
THANKS!!!
 

red

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cert said:
red said:
I know I went into major depression when I found out the my Gold Club heifer tested positive for PHA. She was going to be a donor cow but nixed that idea fast.

Red (cow) (clapping)

Red I have to aplaud you on your decision to not flush the Gold Club heifer. I know that must be hard on your operation but it deserves a pat on the back at the very least. We need more folk like you in the industry. Then TH and PHA would not be as big of an issue.
THANKS!!!

Thanks Cert! & welcome to the group. (welcome)
It wasn't a really big descion, we decided that if she test positive we wouldn't flush her. But I can't say it was a happy choice!
Question for some of you- should carrier animals be banned from sales that the associations or state associations promote?
My vote is yes. The breed association want to promote the "best" their breeds have. I don't honestly believe that a carrier is the "best".
Red
 

phoebe

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This stuff is a little over my head, even though we are starting to talk about genes in biology. 

How many cows are affected?  Is it like 1 in 100, 1 in 10000, or 1 in 100000

How much has it grown as of recent?  I really appreciate the experts and education on this subject.
 

DL

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Hey Phoebe - there are a couple of articles that I think the steerplanet guru's are going to post that may help - or email me and I can send them to you.

The short answer is that we don't know! If you get an SEK Genetic Horizon catalog or look on their web site they list the status (PHA and TH) of most of the popular Shorthorn, Maine, and composite sires.  A high number of them are carriers of one or both defects and many are used heavily (or almost exclusively) in the club calf world. Re TH most traces to the bull Deerpark Improver, a very small percentage trace to a bull called Outcast. Re PHA Draft Pick, Stinger, and Payback appeared to obtain the defective gene at the same time. Stinger is responsible for most but not all the PHA in Shorthorns. Some Shorthorn sires - for example Double Stuff- trace to both Improver and Stinger and test positive for both defects.

So some herds that have heavily used carrier bulls or flushed carrier cows are likely to have a higher (whatever that means) number of carriers than other herds. There is a list on the Shorthorn web site listing carrier and free (TH) animals but of course the numbers are scewed so I don't know if we will ever know!

In terms of "grown" recently - that is an interesting question - TH was seen in Shorthorns I believe for 15 or 20 years and basically ignored by the association - so it isn't new - it is just newly recognized as an issue within the breed and within some composite animals - I think that people have been dunping defective calves either because they wanted to ignore the issue or had no idea what was going on (but lets get real if you have 2 dead calves with the same defect wouldn't you think there was an issue and you should maybe investigate it??)  I think a critical mass of TH calves appeared and people decided theyneeded to figure it out - Nick Steinke and Chuck Hannon were 2 of those people who decided to figure out the problem (there were others too) and in collaboration with Dr Beever and the Barrel Racer they were able to determine informed pedigrees (these are pedigrees that have the animal with TH, known carriers (like the parents) and multiple generations)..from these informed pedigrees they identified the gene, validated it and created a test - all in about a year - pretty darn amazing.

The PHA deal has also probably been around for a while, but not as long - people would see these calves and figure they were just "bad luck" monsters. Again with the proliferation of carrier bulls and the carrier females that were heavily flushed a critical mass of carrier animals was created and when crossed PHA reared its ugly head...

As you probably know these are both recessive traits - so if you breed a carrier to a non carrier you have a 50% chance of having a carrier offspring (and 50% chance of normal). If you breed 2 carriers you have a 50% chance of having a carrier, 25% chance of having a normal and 25% chance of having a dead TH or PHA calf. It is like a coin toss - it is the same chance with every mating. Hope this helps some,

DL (cow) (cow) (cow)
 

Joe Boy

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DL and Barrel Racer:

I have a question that just keeps running around in my big head hunting brain substance.  While I was in college I learned about mutations in genes and like the Greek I studied I have forgotten much more than I remember.  Most mutations were not good if I remember correctly.  What is it that causes these genetic defects to materialize in our generation?  Cattle have been around since before man, and only in the last couple of years have we seen such an outbreak of problems.  Were these problems covered up..... I know some were, as a Shorthorn breeder told me that he had one once in a while but it was just one of those things.  That was 3 years ago and two years ago I started noticing more talk about the problem, but not until your articles did I start to learn how horrible this really was.  I have been blessed and do not have any mature cows who are carriers of either or a bull.  I felt better for myself to learn that I had not sold any carriers as bulls to others.  So, has this always been around or did a mutation in the gene happen because of line breeding?
 

DL

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Hey Joe Boy - the Barrel Racer might have a more erudite description - but these are my thoughts

TH - yeah it was covered up by the ASA for a while, and probably covered up by certain breeders - but we trace the original deletion to Improver a bull imported to the US around the early 70's - we needed to created a certain number of carrier animals who would be mated to carriers and  end up with a certain number of TH calves so that there was (1) concern and (2) the thought that this could actually be a genetic disorder. Then we needed people with affected calves to step up to the plate and provide pedigrees and samples. Dr Hannon was "our man in the field" and many of the Indiana/Illinois Shorthorn breeders graciously provided samples and pedigrees.

PHA - I think the scenario is similar - although I believe that the AMAA did not attempt to hide the issue (although certain breeders may have). The first carrier bull we know of is Paramount  a 1973 full blood MA. Now we know Draft Pick and Stinger and Payback are all carriers and genetically we believe that they all got the defective gene at about the same time, unfortunately only DP traces to Paramount, which means either the Stinger pedigree is incorrect (say it isn't so) or someone else back further had the defective gene. The pedigree of Payback, a compostie bull, is not very useful. It proved to be much more difficult to obtain samples and pedigrees for the PHA gene hunt - still it was about a year to get the gene and develop the test - quite a remarkable feat! It has been 25 years and they are still looking for the PRA genen in some dog breeds!

SO like TH we needed sufficient number of carrier animal mated with carrier animals to produce PHA calves. There was over the last decade a huge influx  of DP genetics, both in terms of his use as a sire and flushing extensively some DP descendant carrier females - so all of a sudden there were enough PHA calves being born for people to care. And I think when the "little guy" was affected it could no longer be ignored.

What is really amazing to me is the person with 6 cows who had 2  TH and 2 PHA calves, or the person with 20 cows and had 5 PHA calves - that is a huge loss for a small operation. The big guys selling the 6 figure animals apparently can absorb that loss - by like Gypsy and several of our other friends you spend big bucks on a "show heifer" with the that she will be the cornerstone of your breeding program and you have a PHA calf - now what...

I think the bottom line is we created these problems by line breeding ...leave it to a human to create a mess! Have a great night - it was actually above zero today and there was sun! Hope that answers you question, DL
 

Telos

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DL said:
Hey Joe Boy - the Barrel Racer might have a more erudite description - but these are my thoughts

TH - yeah it was covered up by the ASA for a while, and probably covered up by certain breeders - but we trace the original deletion to Improver a bull imported to the US around the early 70's - we needed to created a certain number of carrier animals who would be mated to carriers and  end up with a certain number of TH calves so that there was (1) concern and (2) the thought that this could actually be a genetic disorder. Then we needed people with affected calves to step up to the plate and provide pedigrees and samples. Dr Hannon was "our man in the field" and many of the Indiana/Illinois Shorthorn breeders graciously provided samples and pedigrees.

PHA - I think the scenario is similar - although I believe that the AMAA did not attempt to hide the issue (although certain breeders may have). The first carrier bull we know of is Paramount  a 1973 full blood MA. Now we know Draft Pick and Stinger and Payback are all carriers and genetically we believe that they all got the defective gene at about the same time, unfortunately only DP traces to Paramount, which means either the Stinger pedigree is incorrect (say it isn't so) or someone else back further had the defective gene. The pedigree of Payback, a compostie bull, is not very useful. It proved to be much more difficult to obtain samples and pedigrees for the PHA gene hunt - still it was about a year to get the gene and develop the test - quite a remarkable feat! It has been 25 years and they are still looking for the PRA genen in some dog breeds!

SO like TH we needed sufficient number of carrier animal mated with carrier animals to produce PHA calves. There was over the last decade a huge influx  of DP genetics, both in terms of his use as a sire and flushing extensively some DP descendant carrier females - so all of a sudden there were enough PHA calves being born for people to care. And I think when the "little guy" was affected it could no longer be ignored.

What is really amazing to me is the person with 6 cows who had 2  TH and 2 PHA calves, or the person with 20 cows and had 5 PHA calves - that is a huge loss for a small operation. The big guys selling the 6 figure animals apparently can absorb that loss - by like Gypsy and several of our other friends you spend big bucks on a "show heifer" with the that she will be the cornerstone of your breeding program and you have a PHA calf - now what...

I think the bottom line is we created these problems by line breeding ...leave it to a human to create a mess! Have a great night - it was actually above zero today and there was sun! Hope that answers you question, DL






Adding to DL's comments...  I think when we put too much selection pressure for more product ( more muscle, bone, rib shape, hair etc.) and attempt to do it within a short period of time, within a  generations or two, we tend to use genetics that are extreme in phenotype from the norm of a given population. These extreme genetics sometimes tend to come with some kind of compromise.

When looking through the SEK semen catalog and noticeing the high frequency of TH and PHA carriers, I can't help but think that we humans have created a problem, just to be competitive in producing more product in a shorter period of time.

Unlike other genetic defects, TH and PHA come with some show ring appeal. When show cattle bring more dollars, the question will be... How can we eliminate these defects and still produce cattle that fetch a premium for the producers of these cattle? 

 

genes

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Ok I'll try for a Gina/Cliff's notes on mutations.

A mutation is basically some sort of change in the genome.  Various things can happen, such as single base pairs (just one letter on the page) switching to another letter.  Or insertions or deletions of extra letters - how many letters can vary. 

Mutations are something that happen, not overly frequently, but not extremely rarely either.  Sometimes the mutations may be of no consequence at all, such as if they are in an area that does not code for any product, or if the mutation doesn't change the final product.  Other times they may have an effect, but not a large one obvious to the naked eye.  This is because most traits of interest are controlled by a combination of genes working together, each contributing in their own way.  Research now is picking out some of the mutations that have a fairly significant effect.  These are known as "major genes" or "quanitative trait loci" and are what tests like the Genestar ones are based upon.    (This also brings up the point that, no, not all mutations are "bad".  And most times whether it is "good" or "bad" depends on the environment, or our goals, in the case of produciton animals).

But then there are the cases where the mutation is a big deal...these are ones where the proteins produced are not produced at all, or are so different that it changes how they function.  And then it also has to be a gene that "matters".  To bring in a new example for you guys, the double muscling seen in the Belgian Blue breed is the result of a change in a nucleotide, which creates what's called a "premature stop codon".  This means that the assembly of the protein is stopped earlier than it should, making the protein structure totally different and non-functional as a result.  In this case, it is the myostatin gene that is affected, which normally works to regulate prenatal muscle production (ie, it says when to stop making muscles).

So then we get to the cases like TH and PHA.  These are major mutations obviously, as seem by their drastic effects.  They are recessive in nature (ie, the carriers are normal themselves), and they are obviously harmful.  Thus, they are what are known as "deleterious recessive mutations".  Because you need a defective gene from both dam and sire to be affected, we only see affected animals because of inbreeding.  Remember though, it doesn't necessarily have to be close inbreeding, and that's why we see problems now when the mutations originated with bulls popular years ago. 

Deleterious recessives are not a new phenomenon.  The royal family had this high incidence of hemophelia.......  Holsteins had to go through things like mulefoot, which I believe was basically erraticated by not breeding carriers.  At the time, the carriers were identified by their having affected calves.  The difference is now we have genetic tests available to identify carriers before they are bred.

 

jason

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Thanks for posting all this information - great stuff!  We appreciate the work you do in this subject.  :)
 

JbarL

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dragon lady said:
Well we all know about PHA, recessive genetic disease in cattle, described recently in Maine -Anjou and tracing back to 3 bulls at about the same time (implying that a common ancestor was involved in passing the defective gene to all 3 bulls at the same time).  These bulls are Draft Pick, Stinger and Payback. Dr Beever and his trusty side kick Barrel Racer have identified the gene and the defect and so now we can test for PHA (Hallelujah  ;D)

We have trundled back thru Draft Picks pedigree and found that his sire (Nortex General) and his maternal grand sire (AA Black Gold 500) are PHA free - making his dam a suspect, and low and behold her sire Paramount is a PHA carrier. To date he is the only old Maine bull that is identified as a carrier. ALso interesting is that we cannot connect Draft Picks pedigree with Stingers - although the defect is the same. Payback has an incomplete pedigree.

Big deal, you say, nothing new there, but wait......

Recently a group in Australia described PHA in Dexter cattle ( in Australia are not considered a "hobby" breed but a viable beef producing breed)  - some of whom were of Canadian origin (some of us wondered if we were raising big Dexters or they were raising mini Maines!) BUT guess what ------ (drum roll) the genetic defect in PHA seen in Maines is different from the genetic defect seen in PHA in Dexters (same gene, same protein involved but different defect) ----Now isn't that just so cool and interesting - who said the double helix wasn't fun! Not Watson  (clapping)

So Maine breeders are raising Maines
And Dexter breeders are raising Dexters
and both breeds have PHA
and the genetic defect is different

DL

ps I have a copy of the Dexter paper in the AUstralian Vet J if anyone wants it... (cow) (cow) (cow) (cow)
 
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