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Multiple mechanisms of germ cell loss in the perinatal mouse ovary

¹ Department of Molecular and Integrative Physiology, Center for Reproductive Sciences, 3088 Kansas Life Science Innovations Center, University of Kansas Medical Center, KLSIC Room 3016, 3901 Rainbow Boulevard, Kansas City, Kansas 66160, USA² Unidade de Biologia da Reprodução, Instituto de Medicina Molecular and Instituto de Histologia e Biologia do Desenvolvimento, Faculdade de Medicina da Universidade de Lisboa, Avenue Professor Egas Moniz, 1649-028 Lisbon, Portugal³ Marine Biological Laboratories, Woods Hole, Massachusetts 02543, USA

Correspondence should be addressed to D F Albertini; Email: dalbertini{at}kumc.edu

In the perinatal ovary of most mammals, external and internal factors establish a primordial follicle reserve that specifies the duration of the reproductive lifespan of a given species. We analyzed the mechanism of follicle loss and survival in C57BI/6 mice using static and dynamic assays of apoptosis, autophagy, and ovarian morphogenesis. We confirm an initial loss soon after birth, when about 44% of the germ cells detectable at the end of the fetal period abruptly disappear. The observations that (1) few germ or somatic cells were apoptotic in newborn ovaries, (2) vitally stained organ cultures exhibit active extrusion of non-apoptotic germ cells and (3) germ-cell lysosome amplification occurs at birth suggested that additional mechanisms are involved in perinatal germ cell loss. Newborn mouse ovaries cultured in the pH sensitive dye lysotracker red exhibit an increased incidence of acidified non-apoptotic germ cells when maintained in the absence but not in the presence of serum, implying a role for autophagy in germ cell attrition. Inhibitors of autophagy, but not apoptosis, reduce germ cell acidification induced by serum starvation in ovary organ cultures and protein mediators of both autophagy and apoptosis are expressed at birth. From these findings we suggest that multiple perinatal mechanisms establish the primordial follicle reserve in mice.

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