Histone variant H2A.Z and linker histone H1 influence chromosome condensation in Saccharomyces cerevisiae.

Autor:	Rogers AM; Department of Molecular Biology and Biochemistry, Wesleyan University, Middletown, CT 06459, USA., Neri NR; Department of Molecular Biology and Biochemistry, Wesleyan University, Middletown, CT 06459, USA., Chigweshe L; Department of Molecular Biology and Biochemistry, Wesleyan University, Middletown, CT 06459, USA., Holmes SG; Department of Molecular Biology and Biochemistry, Wesleyan University, Middletown, CT 06459, USA.
Jazyk:	angličtina
Zdroj:	Genetics [Genetics] 2024 Apr 03; Vol. 226 (4).
DOI:	10.1093/genetics/iyae022
Abstrakt:	Chromosome condensation is essential for the fidelity of chromosome segregation during mitosis and meiosis. Condensation is associated both with local changes in nucleosome structure and larger-scale alterations in chromosome topology mediated by the condensin complex. We examined the influence of linker histone H1 and variant histone H2A.Z on chromosome condensation in budding yeast cells. Linker histone H1 has been implicated in local and global compaction of chromatin in multiple eukaryotes, but we observe normal condensation of the rDNA locus in yeast strains lacking H1. However, deletion of the yeast HTZ1 gene, coding for variant histone H2A.Z, causes a significant defect in rDNA condensation. Loss of H2A.Z does not change condensin association with the rDNA locus or significantly affect condensin mRNA levels. Prior studies reported that several phenotypes caused by loss of H2A.Z are suppressed by eliminating Swr1, a key component of the SWR complex that deposits H2A.Z in chromatin. We observe that an htz1Δ swr1Δ strain has near-normal rDNA condensation. Unexpectedly, we find that elimination of the linker histone H1 can also suppress the rDNA condensation defect of htz1Δ strains. Our experiments demonstrate that histone H2A.Z promotes chromosome condensation, in part by counteracting activities of histone H1 and the SWR complex. Competing Interests: Conflicts of interest The authors declare no conflict of interest. (© The Author(s) 2024. Published by Oxford University Press on behalf of The Genetics Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)
Databáze:	MEDLINE
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