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E2F Deregulation Compromises ER homeostasis by Attenuating IRE1 Activity

ABSTRACT: The E2F family of transcription factors is an essential regulator of the cell cycle across all metazoan and is often deregulated in cancer. While their primary function is in cell cycle control, E2Fs also influence various cellular processes, such as apoptosis and metabolism. Previous studies in mice have shown that E2F deregulation particularly affect exocrine tissues such as the salivary gland and pancrease. However, the mechanisms behind exocrine cell sensitivity to E2F loss remain inadequately explored. Our lab recently discovered a novel alternatively spliced isoform of Drosophila de2f1, de2f1b, with an additional 16 amino acids than the canonical isoform of de2f1, de2f1a. de2f1b mutants have defects in development of polyploid tissues such as larval salivary glands (SG). Interestingly, SGs of de2f1b mutant shows DNA damage, accumulate cytoplasmic DNA and activation of immune response. This RNA-seq study is to create a gene expression profile of the de2f1b SGs to get a comprehensive understanding of the effects of de2f1b mutation in exocrine tissues.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE294319 | GEO | 2025/09/01

REPOSITORIES: GEO

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Project description:Recent genome-scale ChIP-chip studies of transcription factors have shown that a low percentage of experimentally determined binding sites contain the consensus motif for the immunoprecipitated factor. In most cases, differences between in vivo target sites that contain or lack a consensus motif have not been explored. We have previously shown that most sites to which E2F family members are bound in vivo do not contain E2F consensus motifs. The main purpose of this study was to develop an understanding of how E2F binding specificity is achieved in vivo. In particular, we have addressed how E2F family members are recruited to core promoter regions that lack a consensus motif and are excluded from other regions that contain a consensus motif. Using promoter and ENCODE arrays, we have shown that the predominant factors specifying whether E2F is recruited to an in vivo binding site are a) the site must be in a core promoter and b) the promoter region must be utilized as a promoter by the transcriptional machinery in that particular cell type. We have tested three models for recruitment of E2F to core promoters lacking a consensus site, including a) indirect recruitment, b) looping to the core promoter mediated by an E2F bound to a distal consensus motif, and c) assisted binding of E2F to a site that weakly resembles an E2F consensus motif within the core promoter. To test these models, we developed a new in vivo assay, termed eChIP, which allows analysis of transcription factor binding to isolated promoter fragments. Our findings suggest that in vivo a) the presence of a consensus motif is not sufficient to recruit E2Fs, b) E2Fs can bind to isolated regions that lack a consensus motif, and c) binding can require regions other than the best match to the E2F PWM in the core promoter. Keywords: E2F, ChIP-chip, transcription factor binding, consensus motifs 37 ChIP-chip arrays (of these, 14 array sets are biological duplicates). 22 samples are included in this series, the rest can be found in supplementary info to the following papers: Xu 2007, Jin 2006, Komashko 2008

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E2F Deregulation Compromises ER homeostasis by Attenuating IRE1 Activity

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