The Notch pathway plays an important role in ovary development in invertebrates 
like Drosophila. However its role for the mammalian ovary is unclear. Mammalian 
Hes genes encode transcriptional factors that mediate many of the activities of 
the Notch pathway. Here, we have studied the function of Hes1 during embryonic 
development of the mouse ovary. We find that Hes1 protein is present in somatic 
cells and oocyte cytoplasm and decreases between E15.5 and P0. Conventional Hes1 
knock-out (KO), Hes1 conditional KO in the ovarian somatic, and chemical 
inhibition of Notch signaling decrease the total number, size and maturation of 
oocytes and increase the number of pregranulosa cells at P0. These defects 
correlate with abnormal proliferation and enhanced apoptosis. Expression of the 
proapoptotic gene Inhbb is increased, while the levels of the antiapoptotic and 
oocyte maturation marker Kit are decreased in the Hes1 KO ovaries. Conversely, 
overactivation of the Notch pathway in ovarian somatic cells increases the 
number of mature oocytes and decreases the number of pregranulosa cells. 
Fertility is also reduced by either Hes1 deletion or Notch pathway 
overactivation. In conclusion, our data suggest that the Notch-Hes1 pathway 
regulates ovarian somatic cell development, which is necessary for oocyte 
survival and maturation.