Establishment of the pool of primordial follicles is essential for reproduction. Shortly after their formation, female germ cells undergo a series of incomplete cell divisions resulting in clusters called cysts. After birth, mouse germ cell cysts break down into individual oocytes (a process referred to as cyst breakdown) that are surrounded by somatic pre-granulosa cells to form primordial follicles. During the process of cyst breakdown, a subset of oocytes in each cyst dies with only a third of the initial number of oocytes surviving. The mechanisms controlling cyst breakdown and programmed cell death are unknown. Previous studies have focused on the treatment of neonatal mice with estrogenic compounds and the effect this has in the adult ovary. Estrogen signals are received by two receptors: Estrogen receptor alpha (ERα) and Estrogen receptor beta (ERβ). The purpose of my thesis is to try to understand the role of estrogen signaling through ERβ in the neonatal ovary. Mutant mice lacking ERβ were obtained and examined for defects in cyst breakdown, germ cell death and follicle development. Ovaries were gathered from neonates during cyst breakdown of wild type B6 control (+/+), and ER heterozygous (+/-) and homozygous mutant knockout mice (-/-). ERβ knockout mice exhibited no detrimental effect in cyst breakdown or total oocyte numbers. Follicle development results were inconclusive and further analysis is necessary. These data add to the understanding of mechanisms of cyst breakdown. Ultimately, we hope this will provide a better understanding of oocyte development
