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.