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The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination

ABSTRACT: INO80 is an evolutionary conserved nucleosome remodelling complex that acts in transcription, replication and genome stability. It is required for resistance against genotoxic agents and involved in the repair of DNA double-strand breaks (DSB) by homologous recombination (HR). However, causes underlying the HR defect of INO80-C mutant cells have been controversially discussed. We here unite previous findings using a high-resolution system to study HR in the yeast Saccharomyces cerevisiae. We find that INO80-C has at least two distinct functions during HR, which promote DNA end resection and presynaptic filament formation, respectively. Importantly, specifically the second function is linked to the histone variant H2A.Z. In the absence of H2A.Z, presynaptic filament formation and HR are restored in INO80-C-deficient mutants, suggesting that presynaptic filament formation is the crucial INO80-C function during HR.

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE95801 | GEO | 2017/05/14

SECONDARY ACCESSION(S): PRJNA378431

REPOSITORIES: GEO

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Saccharomyces cerevisiae

Project description:The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination

| PRJNA378431 | ENA

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The INO80 chromatin remodeling complex promotes thermomorphogenesis by connecting H2A.Z eviction and active transcription in Arabidopsis[RNA-seq]

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Anp32e is a histone chaperone that removes H2A.Z from chromatin

Project description:We report a genome wide enrichment, redistribution and accumulation of H2A.Z at specific chromatin control regions, in particular at enhancers and insulators, in mouse embryonic fibroblasts depleted for Anp32e (MEFs Anp32e-/-). H2A.Z ChIP-seq in MEFs WT (+/+) or KO (-/-) for Anp32e.

2014-01-22 | E-GEOD-51579 | biostudies-arrayexpress

Chip-chip from wt and ino80 mutant cells with Htz1

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The histone variant H2A.Z in yeast is almost exclusively incorporated into the +1 nucleosome in the direction of transcription

Project description:To investigate the incorporation dynamics of histone variant H2A.Z, we determined its genomic localization at single nucleosome resolution, as well as the localization of its chromatin remodelers Swr1 and Ino80. We find that Swr1 binding alone is a poor predictor of H2A.Z occupancy levels, and that normal Swr1 and Ino80 localization are actually dependent on H2A.Z. Additionally, we find that H2A.Z’s bimodal incorporation on either side of the NDR is not a general feature of TSS, but is specifically a marker for bidirectional transcription, such that the upstream flanking -1 H2A.Z-containing nucleosome is more appropriately considered as a +1 H2A.Z nucleosome for antisense transcription.

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Symmetric neural progenitor divisions require chromatin-mediated homologous recombination DNA repair by Ino80 [RNA-seq]

Project description:Chromatin regulates spatiotemporal gene expression during neurodevelopment, but it also mediates DNA damage repair crucial to proliferating neural progenitor cells (NPCs). Here, we uncover molecularly dissociable roles for nucleosome remodeler INO80 in chromatin-mediated transcriptome and genome maintenance in corticogenesis. We find that conditional Ino80 deletion from cortical NPCs impairs DNA double-strand break repair, triggering p53 activation, robust apoptosis, and microcephaly, whereas co-deletion of Trp53 with Ino80 leads to remarkable reversal of these phenotypes. Using an in vivo DNA repair assay, we find that Ino80 is selectively required for homologous recombination (HR) DNA repair, which is mechanistically distinct from INO80 function in YY1-associated transcription. Unexpectedly, sensitivity to loss of INO80-mediated HR is dependent on the mode of NPC division: Ino80 deletion causes extensive DNA damage and apoptosis in symmetric NPC-NPC divisions, but not in asymmetric neurogenic divisions. Thus, distinct modes of NPC division have divergent requirements for Ino80-dependent HR DNA repair.

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Symmetric neural progenitor divisions require chromatin-mediated homologous recombination DNA repair by Ino80 [ATAC-seq]

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Chip-chip from wt and ino80 mutant cells with Htz1

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2010-12-01 | E-GEOD-25722 | biostudies-arrayexpress

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