Your browser doesn't support javascript.
loading
What makes a histone variant a variant: Changing H2A to become H2A.Z.
Brewis, Hilary T; Wang, Alice Y; Gaub, Aline; Lau, Justine J; Stirling, Peter C; Kobor, Michael S.
Afiliação
  • Brewis HT; Centre for Molecular Medicine and Therapeutics, BC Children's Hospital Research Institute, Department of Medical Genetics, University of British Columbia, Vancouver, Canada.
  • Wang AY; Centre for Molecular Medicine and Therapeutics, BC Children's Hospital Research Institute, Department of Medical Genetics, University of British Columbia, Vancouver, Canada.
  • Gaub A; Centre for Molecular Medicine and Therapeutics, BC Children's Hospital Research Institute, Department of Medical Genetics, University of British Columbia, Vancouver, Canada.
  • Lau JJ; Centre for Molecular Medicine and Therapeutics, BC Children's Hospital Research Institute, Department of Medical Genetics, University of British Columbia, Vancouver, Canada.
  • Stirling PC; Terry Fox Laboratory, BC Cancer, Department of Medical Genetics, University of British Columbia, Vancouver, Canada.
  • Kobor MS; Centre for Molecular Medicine and Therapeutics, BC Children's Hospital Research Institute, Department of Medical Genetics, University of British Columbia, Vancouver, Canada.
PLoS Genet ; 17(12): e1009950, 2021 12.
Article em En | MEDLINE | ID: mdl-34871303
Chromatin structure and underlying DNA accessibility is modulated by the incorporation of histone variants. H2A.Z, a variant of the H2A core histone family, plays a distinct and essential role in a diverse set of biological functions including gene regulation and maintenance of heterochromatin-euchromatin boundaries. Although it is currently unclear how the replacement of H2A with H2A.Z can regulate gene expression, the variance in their amino acid sequence likely contributes to their functional differences. To tease apart regions of H2A.Z that confer its unique identity, a set of plasmids expressing H2A-H2A.Z hybrids from the native H2A.Z promoter were examined for their ability to recapitulate H2A.Z function. First, we found that the H2A.Z M6 region was necessary and sufficient for interaction with the SWR1-C chromatin remodeler. Remarkably, the combination of only 9 amino acid changes, the H2A.Z M6 region, K79 and L81 (two amino acids in the α2-helix), were sufficient to fully rescue growth phenotypes of the htz1Δ mutant. Furthermore, combining three unique H2A.Z regions (K79 and L81, M6, C-terminal tail) was sufficient for expression of H2A.Z-dependent heterochromatin-proximal genes and GAL1 derepression. Surprisingly, hybrid constructs that restored the transcription of H2A.Z-dependent genes, did not fully recapitulate patterns of H2A.Z-specific enrichment at the tested loci. This suggested that H2A.Z function in transcription regulation may be at least partially independent of its specific localization in chromatin. Together, this work has identified three regions that can confer specific H2A.Z-identity to replicative H2A, furthering our understanding of what makes a histone variant a variant.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Cromatina / Histonas / Adenosina Trifosfatases / Proteínas de Saccharomyces cerevisiae / Galactoquinase Limite: Humans Idioma: En Ano de publicação: 2021 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Cromatina / Histonas / Adenosina Trifosfatases / Proteínas de Saccharomyces cerevisiae / Galactoquinase Limite: Humans Idioma: En Ano de publicação: 2021 Tipo de documento: Article