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FOXL2  mutations cause gonadal dysgenesis or premature ovarian failure (POF) in women, as well as eyelid/forehead dysmorphology in both sexes (the ‘blepharophimosis–ptosis–epicanthus inversus syndrome’, BPES). Here we report that mice lacking  Foxl2  recapitulate relevant features of human BPES: males and females are small and show distinctive craniofacial morphology with upper eyelids absent. Furthermore, in mice as in humans, sterility is confined to females. Features of  Foxl2  null animals point toward a new mechanism of POF, with all major somatic cell lineages failing to develop around growing oocytes from the time of primordial follicle formation.  Foxl2  disruption thus provides a model for histogenesis and reproductive competence of the ovary.

Foxl2 disruption causes mouse ovarian failure by pervasive blockage of follicle development