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Consistent with this view is the observation that a number of mutations at both the white spotting and steel loci have severe reproductive phenotypes in mice, whereas even though a number of human diseases have been associated with defects in these genes, none have been described with reproductive phenotypes. Furthermore, Fortune et al. in a review quote data to indicate that KITL does not promote follicle activation in bovine ovarian cortical explants. Primordial follicle activation is characterized by granulosa cell proliferation and morphogenesis, as well as oocyte growth. Given that granulosa cells do not express the KIT receptor, the signal to coordinate these activities in recombinant mouse KITL-stimulated mouse ovaries must therefore be transmitted via the oocyte, although the identity of such a signal is unknown. Studies describing the temporal expression patterns for KITL and KIT suggest that under normal in vivo conditions KITL availability may be a limiting factor in follicle activation. Only minimal expressions of Kitl mRNA and protein are detectable in murine primordial follicle granulosa cells, and increased expression is observed in follicles enclosed by cuboidal granulosa cells. In contrast, all mouse primordial follicles express KIT mRNA and protein, indicating that every oocyte is potentially responsive to KITL-induced growth and activation.