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Exercise intolerance gene mutation identified

Posted June 11, 2024

By Lindsay Upperman, Ph.D., RAAA director of breed improvement

A new genetic mutation was identified at the University of Nebraska-Lincoln with composite calves, made up of a cross of Red Angus, Simmental and Gelbvieh. The calves in the UNL herd were experiencing exercise intolerance that was exacerbated by stress. For instance, when the herd was being moved to a different pasture, the affected calves tended to not keep up with the herd. They would exhibit muscle fatigue and twitching that would often lead to them laying down or collapsing. After rest, these calves were able to recover and perform normally. In a percentage of cases with extreme or repeated physical exertion the condition can be fatal.

After further research into the genome of these calves, an autosomal recessive genetic defect was identified. This means that both parents of affected calves must carry one copy of the mutation. The affected calves had a change in their genome that caused the PYGM gene to not be developed properly. The PYGM gene produces an enzyme that is used to break down glycogen to ultimately produce energy in muscle cells. The mutation prevented this enzyme from being produced. Furthermore, when taking these affected calves to slaughter, their meat pH was higher than the normal range. A high pH often results in the affected carcass being labeled a dark cutter. Carrier animals showed normal meat pH and meat quality.

Based on the pedigree of the animals utilized at UNL, a common ancestor was found. After testing, the confirmed carrier was BASIN HOBO 79E RAAA #492175. Unfortunately, due to not having available samples on the dam and sire of this carrier, we do not know the status of the parents. The UNL herd also had 4 progeny that were identified as carriers. At this time, no other similar abnormalities have been identified or reported to RAAA within the Red Angus breed.

Sires that have been tested FREE of the mutation include:

RAAA# Name
1260155 BUF CRK THE RIGHT KIND U199
1379610 BROWN PREMIER X7876
1406779 RED SOO LINE POWER EYE 161X
1436844 BIEBER ROLLIN DEEP Y118
1506922 ANDRAS NEW DIRECTION R240
1506931 ANDRAS FUSION R236
1549933 5L DEFENDER 560-30Z
1617230 BIEBER SPARTACUS A193
1619642 3SCC DOMAIN A163
1628086 WFL MERLIN 018A
1683223 H2R PROFITBUILDER B403
1694338 BIEBER DEEP END B597
1701553 5L BLOCKADE 2218-30B
1703720 BROWN ORACLE B112
1725110 PIE CINCH 4126
3491307 RREDS SENECA 731C
3494126 HXC ALLEGIANCE 5502C
3494198 HXC DECLARATION 5504C
3555188 9 MILE FRANCHISE 6305
3751659 BIEBER CL STOCKMARKET E119
3775477 WFL PROFITMAKER E7030
3861137 COLLIER FINISHED PRODUCT
3958815 BIEBER CL ENERGIZE F121

 

At this time, we are currently developing a stand-alone test for this mutation with Neogen. Once the test is developed, other sire lines will be tested to identify the prevalence of this mutation in the Red Angus Breed.

If you have any questions or would like further details on this mutation, please contact the Dr. Lindsay Upperman, RAAA director of breed improvement at lindsay@redangus.org or 940-387-3502 ext. 29. The paper describing this defect can be found here. Thank you to the staff and students at UNL that worked on this: Mackenzie Batt, Leila Venzor, Rachel Reith, Nicolas Herrera, Dr. Jessica Petersen, Dr. Matt Spangler, Dr. Gary Sullivan, and Dr. David Steffen.