ARS | Publication request: EXPRESSION OF MRNA FOR GROWTH HORMONE RECEPTOR, IGF-I, FSH RECEPTOR, AND LH-RECEPTOR IN TESTIS TISSUE OF ANGUS, BRAHMAN, AND ROMOSINUANO BULLS

Submitted to: Journal of Animal Science
Publication Type: Abstract Only
Publication Acceptance Date: July 1, 2002
Publication Date: July 1, 2002

Technical Abstract: Whether genotype influences testis gene expression in temperate Bos taurus (Angus; A; n=10), tropical Bos taurus (Romosinuano; R; n=10), and tropical Bos indicus (Brahman; B; n=8) bulls was evaluated. Bulls were slaughtered 69 to 111 d after attaining sexual maturity. Testicular tissues were collected for mRNA analyses at slaughter. Tissues were snap frozen in liquid nitrogen and stored at -80C until total RNA was extracted. Testicular expression of mRNA for growth hormone receptor exon 1A (GHR1A), GHR exon 1B (GHR1B), IGF-I, FSH receptor (FSHR) and LH receptor (LHR) was determined via ribonuclease protection assays and quantified via integrated optical density units (IOD). There was no difference among breeds (P > 0.10) in GHR1B or LHR; however, testicular GHR1A differed between A and R (P < 0.001) with A bulls having increased expression (0.02 IOD) as compared to R bulls (0.005 IOD). Brahman bulls were not used in this analysis as the GHR1A was specific to Bos taurus cattle. There tended (P < 0.10) to be a difference in testicular expression of IGF-I mRNA with A bulls having increased expression as compared to B and R bulls (0.045, 0.004, and 0.005 IOD for A, B, and R, respectively). There was a difference (P < 0.02) in FSHR expression with A bulls having greater expression than B or R bulls (0.032, 0.004, and 0.006 IOD for A, B, and R, respectively). No difference was detected between B and R bulls for any of the traits measured. The results of this study indicate that sexually mature, tropically adapted Bos taurus bulls may be more similar to sexually mature, tropically adapted Bos indicus bulls than to sexually mature, temperate Bos taurus bulls in terms of testicular mRNA expression of GHR1A, IGF-I, and FSHR.