Relationship between SnoN expression and mouse follicular development, atresia, and luteinization.

SnoN, which belongs to the ski family of nuclear proteins, is a novel oncoprotein; it can induce both oncogenic transformation and terminal muscle differentiation when expressed at high levels. SnoN is an important regulator of signal transduction of the transforming growth factor beta super-family. The present study determined the ovarian localization and regulation of SnoN protein levels in neonatal mice, and in gonadotropin-induced immature mice during follicular development, atresia, and luteinization. In the postnatal mice, positive staining for SnoN was detected for the first time in the interstitial compartment adjacent to the follicles at 7 days and the pattern of immunostaining remained constant. As theca cells differentiated from the stroma, the theca externa layers stained positively for SnoN, and this immunostaining in the theca externa layers persisted in preantral, antral, and preovulatory follicles, even in atretic follicles. Interestingly, the theca interna layers did not contain detected levels of SnoN until the large antral stage of follicular development. In follicular development, SnoN was not expressed in granulosa cells of the healthy follicles but in those that became atretic. After the initiation of luteinization with hCG, SnoN was detected within the luteinizing granulosa cells, and the levels of SnoN were higher during the luteinization process of granulosa cells. Together, our data indicate that SnoN is expressed in a cell-specific manner during ovarian follicular development, atresia, and luteinization and that SnoN might play essential roles in these physiological processes. The present study is the first to investigate SnoN localization and regulation in mouse ovary.