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Interactions between variant histone H2A.Z and linker histone H1 in budding yeast
Author(s) -
Riggs Julianne,
Huang Junning,
Winston Lisle,
Sica Margauex,
Holmes Scott
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.593.1
Subject(s) - histone h1 , chromatin , histone h2a , biology , histone , histone code , chromatin remodeling , microbiology and biotechnology , chromatin immunoprecipitation , genetics , histone methylation , saccharomyces cerevisiae , nucleosome , gene , dna methylation , gene expression , promoter
Loss of the highly conserved histone variant H2A.Z, encoded by HTZ1 , in budding yeast leads to alterations in genomic integrity, including improper establishment of silencing and defects in chromosome cohesion. We have shown that deletion of HHO1 , the gene encoding linker histone H1, suppresses the silencing and plasmid retention defects observed in Δhtz1 cells. HTZ1 is synthetically lethal or sick with several dozen yeast genes of varying function. To examine the specificity of the H1‐H2A.Z interaction, we performed a synthetic screen to see if deletion of HHO1 could rescue cell viability or growth in Δhtz1 . Our data suggests that loss of H1 can suppress synthetic defects and that this suppression is specific for strains lacking proteins involved in histone deacetylation or ubiquitination. Finally, we have used chromatin immunoprecipitation to establish that strains lacking H2A.Z show reduced association of histone H1 with chromatin. Similarly, strains lacking H1 show reduced association of histone H2A.Z with chromatin. Overall our experiments suggest that loss of H2A.Z triggers an H1‐dependent disruption of normal chromatin structure.