Ataxin-7 promotes Drosophila posterior follicle cell maturation by suppressing yorkie function

Abstract

AbstractAtaxin-7 is a key component of the Spt-Ada-Gcn5-acetyltransferase (SAGA) chromatin-modifying complex that anchors Non-stop/USP22, a deubiquitinase, to the complex, thereby helping to coordinate SAGA’s different activities. Recently, we found that non-stop is required in the Drosophila ovary for expression of Hippo signalling pathway components ex and mer, and polarisation of the actin cytoskeleton during collective epithelial cell migration. Here we show that in addition to being required for collective migration, Ataxin-7 plays an essential role in posterior follicle cells (PFCs) to control epithelial maturation and architecture, as well as body axis specification which depends on correct PFC differentiation. Loss of both the deubiquitinase and acetyltransferase modules of SAGA phenocopy loss of Ataxin-7 in PFCs, demonstrating a redundant requirement for SAGA’s enzymatic modules. Strikingly, loss of yorkie completely suppressed effects of Ataxin-7 loss-of-function in PFCs, indicating that the only essential function of Ataxin-7 in PFCs is to suppress yorkie function. This may have broad relevance to the roles of SAGA and Ataxin-7 in development and disease.