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Deciphering the direct transcriptional targets of the Drosophila Activating transcription factor 3 (Atf3) via ChIp-seq: Atf3 bridges the gap between cell polarity and the nucleus

ABSTRACT: Epithelial structure and function are governed by evolutionarily conserved signaling programs. The Drosophila Activating transcription factor 3 (Atf3) prevents epithelial cell replacement during abdominal morphogenesis, yet its transcriptional targets are unknown. Here we demonstrate that Atf3 positively and negatively regulates target genes central to cytoskeleton dynamics and adhesion. Epithelial clones overexpressing Atf3 are enriched for basolateral proteins at the expense of apical identity. Strikingly, Atf3 functions downstream of the Scrib polarity module. Depleting either scrib or dlg1 induces atf3 expression, while loss of atf3 suppresses differentiation and polarity defects in cells deficient for the Scrib complex

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE71206 | GEO | 2018/02/20

REPOSITORIES: GEO

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Transcriptional response to Activating transcription factor 3 (Atf3) activity in the Drosophila eye antenna imaginal disc (EAD) epithelium.

Project description:Here we describe the transcriptional response to Atf3 expression in the EAD. Atf3 is a cell polarity response gene acting downstream of the membrane-associated Scribble polarity complex. Loss of the neoplastic tumor suppressors Scribble or Dlg1 induces Atf3 expression via aPKC signaling. Using ChIP-seq we have determined that Atf3 targets are enriched for roles in cytoarchitecture. Gain of Atf3 function interferes with organization of the microtubule network, thereby disturbing vesicular trafficking processes including endocytosis, and consequently alters the distribution of key polarity proteins along the apicobasal axis. Conversely, removal of Atf3 from cells lacking Dlg1 suppresses trafficking defects and restores both the normal localization of polarity determinants and epithelial differentiation. These results thus establish loss of polarity as a novel cue that induces Atf3 and demonstrate that gain of Atf3 function drives specific hallmarks of epithelial cells deficient for the Scribble polarity module.

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The exon junction complex regulates the splicing of cell polarity gene dlg1 to control Wingless signaling in development

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The exon junction complex regulates the splicing of cell polarity gene dlg1 to control Wingless signaling in development

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Su(H) ChIP-on-chip of Notch-stimulated overgrowing Drosophila melanogaster wing imaginal discs

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