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

Summary

Drosophila ovary has been used as a model system for a long time to study cellular interactions. In this article, authors have shown that Ataxin-7 which is a component of SAGA chromatin-modifying complex plays a novel role in promoting Drosophila posterior follicle cells (PFC) maturation.

They generated Ataxin loss of function clones in the border cells by MARCM and found that significantly lesser number of border cells were able to migrate towards the oocyte which was found to be due to defective distribution of F-actin at the border cell junctions. Loss of ataxin-7 also caused formation of bi or multi-layered epithelium unlike the wild type, which occurred due to failure in cell cycle progression. Since these defects have been found to arise due to cell polarity defects, the authors looked at several cell polarity determinants and observed non uniform and reduced distribution of Crumbs and aPKC. Finally to find the underlying mechanism or pathways regulating this, the authors looked at Notch signalling, they observed disrupted notch localization and its downstream effectors. ‘Since the SAGA complex consists of two enzymatic modules: a histone acetyltransferase (HAT) and deubiquitinase (DUB) (Weake and Workman, 2012)’, the authors tried to determine if loss of any of the two gave similar phenotypic outcomes. They did not find any abnormality when each was knocked-down one by one, but knockdown of both simultaneously gave results similar to when Ataxin-7 was deleted. Finally they looked at both Notch and Hippo signalling and found that overexpression of Notch

was unable to rescue the defects caused by Ataxin-7 deletion whereas yorkie downregulation rescued some of the defects.