Ataxin-7 promotes Drosophila posterior follicle cell maturation by suppressing yorkie function
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Abstract
Ataxin-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.
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This Zenodo record is a permanently preserved version of a PREreview. You can view the complete PREreview at https://prereview.org/reviews/7034482.
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 …
This Zenodo record is a permanently preserved version of a PREreview. You can view the complete PREreview at https://prereview.org/reviews/7034482.
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.
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