期刊
PLOS GENETICS
卷 8, 期 9, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pgen.1002974
关键词
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资金
- BBSRC
- Babraham Institute for WRW through the Science Policy Committee
- Leonardo Da Vinci project Unipharma-Graduates
- Royal Society [500567]
- Biotechnology and Biological Sciences Research Council [1129000, BB/F020236/1, BBS/E/B/000C0404] Funding Source: researchfish
- Medical Research Council [G0701175] Funding Source: researchfish
- BBSRC [BBS/E/B/000C0404, BB/F020236/1] Funding Source: UKRI
- MRC [G0701175] Funding Source: UKRI
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.
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