Cloning and sequence analysis of the extracellular region of the polar bear (Ursus maritimus) luteinizing hormone receptor (LHr), follicle stimulating hormone receptor (FSHr), and prolactin receptor (PRLr) genes and their expression in the testis of the black bear (Ursus americanus)

2000 
Male black bears undergo seasonal changes in testicular activity. The testes are fully functional from May through July, regress from July through December, and recrudesce from January until May. The mechanisms responsible for the initiation of testicular recrudescence in the bear are unknown. The objectives of this study were to: (1) clone and sequence a substantial fragment of the extracellular portion of the luteinizing hormone receptor (LHr: 646 bp) and follicle stimulating hormone receptor (FSHr: 852 bp), and the extracellular/transmembrane portion of the prolactin receptor (PRLr: 680 bp) in the bear using reverse transcription-polymerase chain reaction (RT-PCR); and (2) determine whether the expression of LH-, FSH-, and PRL-receptor mRNA transcripts differs between the beginning and terminal stages of testicular recrudescence. Comparisons of the partial cDNA and predicted amino acid sequences of ursine receptors with the corresponding sequences from the pig, cow, human, and rat suggest that the LHr and FSHr are highly conserved (LHr: 87.1–93.7%; FSHr: 86.0–92.7%) whereas the PRLr is less well conserved (81–87%). Testicular LHr mRNA was more abundant during the breeding season in May than during the non-breeding season (early stage of recrudescence) in January. In contrast, testicular FSHr mRNA abundance was greater in January than in May. Testicular PRLr mRNA appeared equally abundant in January and May; however, two additional transcripts were present during the breeding season in May. This study provides molecular tools for future investigations of the control of testicular recrudescence in the black bear and demonstrates that the expression of testicular gonadotropin and PRL receptor mRNA is seasonally regulated. Mol. Reprod. Dev. 55:136–145, 2000. © 2000 Wiley-Liss, Inc.
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