Wash exhibits context-dependent phenotypes and, along with the WASH regulatory complex, regulates oogenesis.

WASH, a Wiskott-Aldrich syndrome (WAS) family protein, has many cell and developmental roles related to its function as a branched actin nucleation factor. Similar to mammalian WASHC1, which is embryonic lethal, Wash was found to be essential for oogenesis and larval development. Recently, however, was reported to be homozygous viable. Here, we verify that the original null allele harbors an unrelated lethal background mutation; however, this unrelated lethal mutation does not contribute to any Wash oogenesis phenotypes. Significantly, we find that: (1) the homozygous null allele retains partial lethality, leading to non-Mendelian inheritance; (2) the allele's functions are subject to its specific genetic background; and (3) the homozygous stock rapidly accumulates modifications that allow it to become robust. Together, these results suggest that Wash plays an important role in oogenesis via the WASH regulatory complex. Finally, we show that another WAS family protein, SCAR/WAVE, plays a similar role in oogenesis and that it is upregulated as one of the modifications that allows the allele to survive in the homozygous state.