RUMOR - Jakes proud jazz mulefoot carrier??

[Young]

I just heard jakes proud jazz is having several calves born with mulefoot.  Anyone else heard or seen this?

 

[kfacres]

  ???  o NO, not at this time, especially of this time of year..> O NO< not the savior??  can't be/// (thumbsup)

 

[ruhtram]

Dang this would really suck

 

[knabe]

simple recessive.

if he's great, it won't be a problem with screening.

http://www.holsteinusa.com/programs_services/genetic_services.html

hopefully the mutation is the same?

 

[kfacres]

simple recessive.

if he's great, it won't be a problem with screening.

http://www.holsteinusa.com/programs_services/genetic_services.html

hopefully the mutation is the same?

I knew that was in the Holstein breed-- has been for a very long time...  I remember way back that we were using bulls which had carriers of that in their lineage... 

Interesting part is that genetic test- is way more expensive than any other (except the $100 one)

 

[sue]

I'm not sure if the defect is mulefootor not, but I heard a rumour back in mid summer that the JPJ lin possibly had a defect. When I asked reps from the ASA they originally said they would not comment but they later said they were presently collecting information and it did look like there was a definite defect. I'm sure more will come out in time.

ditto

 

[aj]

Historically have the Irish shorthorns ever show a mulesfoot defect?

 

[trevorgreycattleco]

Dag gone. This is going to stress alot of folks out. He sired 1305 registered calves last year. The next 6 bulls on the list are all Trumps. Then Ace of Diamonds and Goldmine 2109. Even if you didnt like him, he has been good for the breed. Easy to manage or not, this is just bad news all the way around. Not the end of the world but a shot to the chops for sure.

 

[aj]

At some point the breed will not be able to breed around the defects. A defect is a defect.

 

[DL]

There are multiple mutations involved in mule foot - it is a monogenic recessive with incomplete penetrance from Theriogenology 70 (2008) 535–549

Syndactyly in cattle is also called ‘‘mulefoot’’ and refers to the fusion or non-division of the two functional digits of the bovine foot with synostotic (fusion of normally separate skeletal bones) phalanges. Phalanges are synostotic horizontally and by pairs; the second pair of phalanges is most fully synostotic, followed by the third, and then the first. This abnormality is often subject to a right-left and a front-rear gradient, being most often seen in the front and right feet. Proximal limb structures can also be affected in syndactylous animals, resulting in a reduced number of sesamoid bones. Synostotic phalanges can be detected as early as 37–40 d post-coitum in the bovine embryo.

Bovine syndactyly is an autosomal monogenic recessive trait with incomplete penetrance (79% in Holstein cattle) and variable expression. Crossbreeding experiments between Holstein and Aberdeen-Angus have produced syndactylous progeny, suggesting a common locus responsible for the disorder in both breeds. The bovine syndactyly locus was localized to chromosome 15 in 1996 [59] and is due tomutation in the low-density lipoprotein receptor-related protein 4 gene (LPR4). The occurrence of syndactylous cattle peaked in the 1970s as carrier animals were indirectly selected for superior production of milk and butterfat. The development of test mating and genetic testing greatly reduced the incidence of syndactyly. Unfortunately, syndactylous animals are still occasionally observed in the Holstein population and some carrier animals are still being used for breeding. Eradication of syndactyly will require a precise method to detect the causal genetic mutation. Unfortunately there is extensive allelic heterogeneity in LPR4, with the six independent mutations described still not accounting for all analyzed cases. The two most frequent mutations are the Holstein-specific exon 33 mutation and the Angus-specific exon 37 mutation. Because not all causal mutations have been detected, genetic testing for the carrier status of single individuals remains difficult. Several labs offer testing for the known genetic mutations [Germany (http://www.tieraerztliches-institut.uni-goettingen. de/); Italy (http://www.lgscr.it/eng/index.htm); France (http://www.labogena.fr/); the Netherlands (http://www.vhlgenetics.com/vhl/index.html)]. Unfortunately, each laboratory utilizes different technologies and seldom analyze for the same genetic mutations.

The American Angus Association lists the status of several bulls and cows as carrier or free of the mutations responsible for syndactyly. However, this freedom from carrier status is based solely on progeny test information, and could be questioned in the context of the allelic heterogeneity of syndactyly in Holstein cattle.

 

[aj]

Ouch...thats not as simple as th and pha then?

 

[knabe]

There are multiple mutations involved in mule foot - it is a monogenic recessive with incomplete penetrance from Theriogenology 70 (2008) 535–549

ouch.  sure would be nice to know why there are these multiple mutations in genes like this one and double muscling and why the mutations are not equally distributed in all simple recessive genes.  must have something to do with how the animals moved around.  would like to have crossover points mapped with mutation rates.

started reading about this.  seems like a good compact molecular biology course.

 

[knabe]

maybe it's not such a bad thing.

http://www.voxmagazine.com/stories/2011/08/04/missouri-farmers-preserve-rare-pig-breed/

The meat from these domesticated, castrated male pigs isn’t common pork. This pork is sensational, the Gelders say. It’s flavorful, fatty and juicy. It’s red and marbled like beef. They say it tastes like pork from 50 years ago, before the industrialization of agriculture turned pork into “the other white meat.”

 

[oakview]

Interesting that Holstein and Angus are mentioned in the recent history of mulefoot.  Wasn't there an "Angus" bull in the 70's that went by the nickname of "Sport" that was a mulefoot carrier?

 

[sue]

There are multiple mutations involved in mule foot - it is a monogenic recessive with incomplete penetrance from Theriogenology 70 (2008) 535–549

Syndactyly in cattle is also called ‘‘mulefoot’’ and refers to the fusion or non-division of the two functional digits of the bovine foot with synostotic (fusion of normally separate skeletal bones) phalanges. Phalanges are synostotic horizontally and by pairs; the second pair of phalanges is most fully synostotic, followed by the third, and then the first. This abnormality is often subject to a right-left and a front-rear gradient, being most often seen in the front and right feet. Proximal limb structures can also be affected in syndactylous animals, resulting in a reduced number of sesamoid bones. Synostotic phalanges can be detected as early as 37–40 d post-coitum in the bovine embryo.

Bovine syndactyly is an autosomal monogenic recessive trait with incomplete penetrance (79% in Holstein cattle) and variable expression. Crossbreeding experiments between Holstein and Aberdeen-Angus have produced syndactylous progeny, suggesting a common locus responsible for the disorder in both breeds. The bovine syndactyly locus was localized to chromosome 15 in 1996 [59] and is due tomutation in the low-density lipoprotein receptor-related protein 4 gene (LPR4). The occurrence of syndactylous cattle peaked in the 1970s as carrier animals were indirectly selected for superior production of milk and butterfat. The development of test mating and genetic testing greatly reduced the incidence of syndactyly. Unfortunately, syndactylous animals are still occasionally observed in the Holstein population and some carrier animals are still being used for breeding. Eradication of syndactyly will require a precise method to detect the causal genetic mutation. Unfortunately there is extensive allelic heterogeneity in LPR4, with the six independent mutations described still not accounting for all analyzed cases. The two most frequent mutations are the Holstein-specific exon 33 mutation and the Angus-specific exon 37 mutation. Because not all causal mutations have been detected, genetic testing for the carrier status of single individuals remains difficult. Several labs offer testing for the known genetic mutations [Germany (http://www.tieraerztliches-institut.uni-goettingen. de/); Italy (http://www.lgscr.it/eng/index.htm); France (http://www.labogena.fr/); the Netherlands (http://www.vhlgenetics.com/vhl/index.html)]. Unfortunately, each laboratory utilizes different technologies and seldom analyze for the same genetic mutations.

The American Angus Association lists the status of several bulls and cows as carrier or free of the mutations responsible for syndactyly. However, this freedom from carrier status is based solely on progeny test information, and could be questioned in the context of the allelic heterogeneity of syndactyly in Holstein cattle.

Thanks DL ! I now understand this a little better.

 

[linnettejane]

you have got to be kidding me

 

[kfacres]

you have got to be kidding me

nope... (clapping)  as devastating as it will be to the breed... I still think it's funny...


I just another fellow shorthorn breeder... I for see non papered as the future- as well out outside the box thinking and main stream avoidance.

 

[aj]

Don't see any fun in it cause are there any more lines out there? The AHL Kodiak is an interesting individual.Ahlschwede bred. Is there a triple stuff going here?

 

[trevorgreycattleco]

I wonder if JSF has a bunch of JPJ sons selling in Denver? Is the catalog out yet? Timing on this is about as bad as you could ask for. Back to the drawing board for alot of folks.  This sucks.

 

[aj]

Well for starters it may just be rumour. There is always confusion on defects. Th and pha were confused with each other till it was decided they were seperate deals. Could have been a poison weed or something a cow ate also to have a deformed calf.