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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Embryonic Development, Female, Germ Cells, Homeodomain Proteins, Mice, Mice, Inbred C57BL, Mice, Mutant Strains, Oogonia, Ovarian Follicle, Ovary, Pregnancy, Primary Ovarian Insufficiency, Transcription Factors.
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Is premature ovarian failure in nobox-deficient mice caused by defects in somatic cell invasion and germ cell cyst breakdown? Context: To understand the mechanism of premature ovarian failure (POF). The ultrastructural (electron microscopy) analysis of primordial ovarian follicles in Nobox deficient mice. 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.
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These results indicate that POF syndrome in Nobox deficient mice results from the faulty signaling between somatic and germ line components during embryonic 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. Final Decision: yes