SWI/SNF-like chromatin remodeling factor Fun30 supports point centromere function in S. cerevisiae
journal contributionposted on 2023-06-08, 14:56 authored by Mickaël Durand-Dubief, William Ryan Will, Edoardo Petrini, Delphine Theodorou, Rachael R. Harris, Margaret R. Crawford, Konrad Paszkiewicz, Felix Krueger, Rosa Maria Correra, Anna T. Vetter, J. Ross Miller, Nicholas A. Kent, Patrick Varga-Weisz
Budding yeast centromeres are sequence-defined point centromeres and are, unlike in many other organisms, not embedded in heterochromatin. Here we show that Fun30, a poorly understood SWI/SNF-like chromatin remodeling factor conserved in humans, promotes point centromere function through the formation of correct chromatin architecture at centromeres. Our determination of the genome-wide binding and nucleosome positioning properties of Fun30 shows that this enzyme is consistently enriched over centromeres and that a majority of CENs show Fun30-dependent changes in flanking nucleosome position and/or CEN core micrococcal nuclease accessibility. Fun30 deletion leads to defects in histone variant Htz1 occupancy genome-wide, including at and around most centromeres. FUN30 genetically interacts with CSE4, coding for the centromere-specific variant of histone H3, and counteracts the detrimental effect of transcription through centromeres on chromosome segregation and suppresses transcriptional noise over centromere CEN3. Previous work has shown a requirement for fission yeast and mammalian homologs of Fun30 in heterochromatin assembly. As centromeres in budding yeast are not embedded in heterochromatin, our findings indicate a direct role of Fun30 in centromere chromatin by promoting correct chromatin architecture.
- Published version
PublisherPublic Library of Science
Department affiliated with
- Sussex Centre for Genome Damage Stability Publications
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