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Biology of Reproduction 65, 119-127 (2001)
© 2001 Society for the Study of Reproduction, Inc.


Regular Article

Expression of Stress Response Genes in Germ Cells During Spermatogenesis1

Adriana Aguilar-Mahechac, Barbara F. Halesc, and Bernard Robaire2,d

c Departments of Pharmacology and Therapeutics, and d of Obstetrics and Gynecology, McGill University, Montreal, Quebec, Canada H3G 1Y6

ABSTRACT

During germ cell development different spermatogenic cell types show remarkable variation in their susceptibility to stressful stimuli. Various cellular mechanisms are triggered in germ cells after exposure to stress, but the expression of only a few of the genes involved in such pathways has been studied during spermatogenesis. In the present study we determined the expression profiles of 216 stress response genes in isolated rat germ cells (pachytene spermatocytes, and round and elongating spermatids) using cDNA atlas arrays. Of the 216 genes studied, 86 were detected in pachytene spermatocytes, 82 in round spermatids, and 52 in elongating spermatids. Fifty percent (48) of the total number of genes detected during spermatogenesis were detected in all three cell types while nearly 25% (25) were expressed exclusively in pachytene spermatocytes and round spermatids; some cell specific transcripts were observed also. The use of the K means clustering method allowed us to group genes by their pattern of expression during spermatogenesis; five specific expression profiles were obtained and analyzed. To determine how stress response genes are regulated throughout spermatogenesis, we examined the expression of genes involved in stress response mechanisms such as heat shock proteins-chaperones, DNA repair, and oxidative stress. Genes belonging to these families were differentially expressed during germ cell development. We suggest that the differential expression of stress response genes during spermatogenesis contributes to the selectivity of the susceptibility of germ cells to stress.

FOOTNOTES

First decision: 16 January 2000.

1 Supported by a grant from the Canadian Institutes of Health Research.

2 Correspondence: B. Robaire, Department of Pharmacology and Therapeutics, McGill University, 3655 Promenade Sir-William-Osler, Montréal, PQ, Canada H3G 1Y6. FAX: 514 398 7120; brobaire{at}pharma.mcgill.ca




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