Durand-Dubief, Mickaël, Will, William Ryan, Petrini, Edoardo, Theodorou, Delphine, Harris, Rachael Rebecca, Crawford, Margaret Rosemary, Paszkiewicz, Konrad, Krueger, Felix, Correra, Rosa Maria, Vetter, Anna T., Miller, J. Ross, Kent, Nicholas A. ![]() |
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Abstract
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.
Item Type: | Article |
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Date Type: | Publication |
Status: | Published |
Schools: | Biosciences |
Subjects: | Q Science > QH Natural history > QH426 Genetics |
Publisher: | Public Library of Science |
ISSN: | 1553-7404 |
Date of First Compliant Deposit: | 30 March 2016 |
Last Modified: | 06 May 2023 08:13 |
URI: | https://orca.cardiff.ac.uk/id/eprint/47564 |
Citation Data
Cited 35 times in Scopus. View in Scopus. Powered By Scopus® Data
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