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CHRAC/ACF Contribute to the Repressive Ground State of Chromatin

By Alessandro Scacchetti, Laura Brueckner, Dhawal Jain, Tamas Schauer, Xu Zhang, Frank Schnorrer, Bas van Steensel, Tobias Straub, Peter B. Becker

Posted 13 Nov 2017
bioRxiv DOI: 10.1101/218768 (published DOI: 10.26508/lsa.201800024)

The chromatin remodeling complexes CHRAC and ACF combine the ATPase ISWI with the signature subunit ACF1. These enzymes catalyze well-studied nucleosome sliding reactions in vitro, but how their actions affect physiological gene expression is unclear. Here we explored the influence of Drosophila CHRAC/ACF on transcription by complementary gain- and loss-of-function approaches. Targeting ACF1 to multiple reporter genes inserted at many different genomic locations revealed a context-dependent inactivation of poorly transcribed reporters in repressive chromatin. Accordingly, single-embryo transcriptome analysis of a Acf knock-out allele showed that only lowly expressed genes are de-repressed in the absence of ACF1. Finally, the nucleosome arrays in Acf-deficient chromatin show loss of physiological regularity, particularly in transcriptionally inactive domains. Taken together our results highlight that ACF1-containing remodeling factors contribute to the establishment of an inactive ground state of the genome through chromatin organization.

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