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Cellular and molecular mechanisms of heat stress related to bovine ovarian function

Wednesday, July 23, 2014: 4:00 PM
2103C (Kansas City Convention Center)
Zvi Roth , The Hebrew University of Jerusalem, Rehovot, Israel
Abstract Text: In light of the intensive genetic selection for high milk production and the onset of global warming, the reduced fertility of lactating cows during the summer is expected to worsen in coming years. While not entirely clear, the mechanism of fertility reduction appears to be multifactorial in nature, including altered follicular development, depressed follicular dominance, and impaired steroidogenesis and gonadotropin secretion. Heat-induced perturbations in the physiology of the follicle-enclosed oocyte have also been documented, expressed by impaired cleavage rate and reduced developmental competence. Oocyte alterations include increased polyunsaturated fatty acids in the membrane, reactive oxygen species, ceramide formation, caspase activity, and induction of apoptosis via the sphingomyelin and/or mitochondrial pathways. New insight into the cellular and molecular alterations have revealed heat-induced perturbations in both nuclear and cytoplasmic maturation events—meiosis resumption, metaphase-II plate formation, cytoskeleton rearrangement and translocation of cortical granules. Alterations in mitochondrial distribution (i.e., a low proportion of category-I oocytes) and mitochondrial function (low membrane potential) have been recently reported for oocytes collected during the summer. These were associated with impaired expression of both nuclear (SDHD and ATP5B) and mitochondrial (ND2, CYTB, COXII) genes which are crucial in the mitochondrial respiratory chain. In addition, season-induced alteration in maternal-mRNA storage was documented, expressed by reduced transcript levels (C-MOS, GDF9, POU5F1 and GAPDH) in MII-stage oocytes and embryos, before (2-, 4-and 8-cell stages) and after (8–16-cell stage) embryonic genome activation. These findings clarify the association between cellular and molecular modifications and reduced developmental competence during the hot season. This knowledge is essential for developing new approaches to coping with this unsolved problem.

Keywords: heat stress, bovine ovarian function