Premature ovarian failure in nobox-deficient mice is caused by defects in somatic cell invasion and germ cell cyst breakdown

Purpose To understand the mechanism of premature ovarian failure (POF). Methods The ultrastructural (electron microscopy) analysis of primordial ovarian follicles in Nobox deficient mice. Results We studied, for the first time, the fate of oogonia in embryonic (prenatal) mouse ovaries and showed that the abolishment of the transition from germ cell cysts to primordial follicles in the ovaries of Nobox deficient mice is caused by defects in germ cell cyst breakdown, leading to the formation of syncytial follicles instead of primordial follicles. Conclusions These results indicate that POF syndrome in Nobox deficient mice results from the faulty signaling betweensomaticandgermlinecomponentsduringembryonic development. In addition, the extremely unusual and abnormal presence of adherens junctions between unseparated oocytes within syncytial follicles indicates that faulty communication between somatic and germ cells is involved in, or leads to, abnormalities in the cell adhesion program.