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PLoS Genet. 2012 Sep;8(9):e1002974. doi: 10.1371/journal.pgen.1002974. Epub 2012 Sep 27.

SWI/SNF-like chromatin remodeling factor Fun30 supports point centromere function in S. cerevisiae.

Author information

  • 1Nuclear Dynamics, Babraham Institute, Cambridge, United Kingdom.

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.

PMID:
23028372
[PubMed - indexed for MEDLINE]
PMCID:
PMC3459985
Free PMC Article

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