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This Article Accepted manuscript (PDF) All Versions of this Article: JOE-09-0109v1 JOE-09-0109v2 202/3/407    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Chen, Y. Articles by Pepling, M. PubMed PubMed Citation Articles by Chen, Y. Articles by Pepling, M.

Y Chen, Biology, Syracuse University, Syracuse, United States
K Breen, Biology, Syracuse University, Syracuse, United States
M Pepling, Biology, Syracuse University, Syracuse, United States

Correspondence: Melissa Pepling, Email: mepeplin{at}syr.edu

During mouse embryonic development, oocytes develop in germline cysts, formed by several rounds of cell division followed by incomplete cytokinesis. Shortly after birth, cysts break down and individual oocytes are enclosed by granulosa cells to form primordial follicles. At the same time, two thirds of the oocytes die by apoptosis with only one third surviving. We have previously shown that the steroid hormones, estradiol (E2) and progesterone, as well as the phytoestrogen genistein can inhibit cyst breakdown and primordial follicle assembly. However, the mechanisms by which steroid hormones regulate oocyte cyst breakdown and selective oocyte survival are unknown. Here, we confirmed expression of estrogen receptor (ER) mRNA and protein in neonatal mouse ovaries using RT-PCR, Western blotting and immunocytochemistry. We then used estrogen receptor specific agonists and antagonists to understand the mechanism of estrogen signaling. PPT, an ER selective agonist and DPN, an ERβ selective agonist both inhibited cyst breakdown in organ culture, suggesting that E2 can signal through both receptors to regulate cyst breakdown. ICI 182,780, an estrogen receptor antagonist completely blocked E2’s action. MPP, an ER specific antagonist fully blocked E2’s effect on oocyte cyst breakdown and primordial follicle assembly and (R,R)-THC, an ERβ specific antagonist, partially blocked E2, further supporting the idea that both receptors are involved in estrogen signaling in neonatal oocyte development. E2 conjugated to BSA which can only exert effects at the membrane, was able to inhibit cyst breakdown, implying that E2 could also function through a membrane bound estrogen receptor to regulate cyst breakdown.