Myostatin Genotype Regulates Muscle-Specific miRNA Expression in Mouse Pectoralis Muscle

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2010-11-01
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Rachagani, Satyanarayana
Cheng, Ye
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Reecy, James
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Animal Science

The Department of Animal Science originally concerned itself with teaching the selection, breeding, feeding and care of livestock. Today it continues this study of the symbiotic relationship between animals and humans, with practical focuses on agribusiness, science, and animal management.

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The Department of Animal Husbandry was established in 1898. The name of the department was changed to the Department of Animal Science in 1962. The Department of Poultry Science was merged into the department in 1971.

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Loss of functional Myostatin results in a dramatic increase in skeletal muscle mass. It is unknown what role miRNAs play in Myostatin mediated repression of skeletal muscle mass. We hypothesized that Myostatin genotype would be associated with the differential expression of miRNAs in skeletal muscle. Loss of functional Myostatin resulted in a significant increase (p < .001) in miR-1, miR-133a, miR-133b, and miR-206 expression. In contrast, Myostatin genotype had no effect (P > .2) on miR-24 expression level. Myostatin genotype did not affect the expression level of MyoD or Myogenin (P > 0.5). Myostatin may regulates the expression of miRNAs such as miR-133a, miR-133b, miR-1, and miR-206 in skeletal muscle as it has been observed that the expression of those miRNAs are significantly higher in myostatin null mice compared to wild type and heterozygous mice. In contrast, expression of myogenic factors such as MyoD or Myogenin has not been affected by myostatin in the muscle tissue.

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This article is from BMC Research Notes 3 (2010): 297, doi:10.1186/1756-0500-3-297. Posted with permission.

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Fri Jan 01 00:00:00 UTC 2010
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