The distribution of INO80 in the development of heart failure.
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE240179 | GEO | 2024/01/04
REPOSITORIES: GEO
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Project description:The project aimed to investigate the composition/interactome of the human INO80 complex. To this end, INO80B - a core INO80 complex subunit - was endogenously tagged with V5 epitope tag at its C terminus in MCF-7 cells, and co-immunoprecipitation followed by LC-MS/MS analysis was performed using anti-V5 Abs.
2023-12-10 | PXD020712 | Pride
Project description:In order to detect the effect of INO80 on chromatin accessibility, we will utilize the Assay for Transposase Accessible Chromatin with highthroughput sequencing (ATAC-Seq).
2024-01-04 | GSE240178 | GEO
Project description:We mapped 4 subunits of the INO80 complex using ChIP-seq in HepG2 liver cancer cells. We found a subclass of sites occupied by the INO80 ATPase subunit, but not by any accessory subunits that we call 'Non-canonical' INO80 sites. These sites are characterized by repressed chromatin.
2018-01-23 | GSE107730 | GEO
Project description:INO80 is the catalytic subunit of the multi-subunit INO80-chromatin remodeling complex that has been implicated in DNA replication, repair, and transcription regulation. Ino80-deficiency in murine spermatocytes (Ino80cKO) results in pachytene arrest of spermatocytes, due to incomplete synapsis and aberrant DNA double-strand break repair (DSBR) that leads to apoptosis. We explored the mechanism by which INO80 mediates meiotic progression. RNA-seq on Ino80cKO spermatocytes revealed major changes in transcription, indicating that an aberrant transcription program arises upon INO80 depletion. In Ino80WTspermatocytes, genome-wide analysis showed that INO80-binding sites were mostly promoter proximal and necessary for the regulation of spermatogenic gene expression, primarily of premeiotic and meiotic genes. Further, most of the genes poised for activity, as well as those genes that are active, shared INO80 binding. In Ino80cKO spermatocytes, most poised genes demonstrated de-repression due to reduced H3K27me3 enrichment, and in turn showed increased expression levels. INO80 interacts with the core PRC2 complex member SUZ12 and promotes its recruitment. Further, INO80 mediates H2A.Z incorporation at the poised promoters, which was reduced in Ino80cKO spermatocytes. Taken together, INO80 is emerging as a major regulator of the meiotic transcription program by mediating poised chromatin establishment through SUZ12 binding.
2021-12-21 | GSE179579 | GEO
Project description:INO80 is the catalytic subunit of the multi-subunit INO80-chromatin remodeling complex that has been implicated in DNA replication, repair, and transcription regulation. Ino80-deficiency in murine spermatocytes (Ino80cKO) results in pachytene arrest of spermatocytes, due to incomplete synapsis and aberrant DNA double-strand break repair (DSBR) that leads to apoptosis. We explored the mechanism by which INO80 mediates meiotic progression. RNA-seq on Ino80cKO spermatocytes revealed major changes in transcription, indicating that an aberrant transcription program arises upon INO80 depletion. In Ino80WTspermatocytes, genome-wide analysis showed that INO80-binding sites were mostly promoter proximal and necessary for the regulation of spermatogenic gene expression, primarily of premeiotic and meiotic genes. Further, most of the genes poised for activity, as well as those genes that are active, shared INO80 binding. In Ino80cKO spermatocytes, most poised genes demonstrated de-repression due to reduced H3K27me3 enrichment, and in turn showed increased expression levels. INO80 interacts with the core PRC2 complex member SUZ12 and promotes its recruitment. Further, INO80 mediates H2A.Z incorporation at the poised promoters, which was reduced in Ino80cKO spermatocytes. Taken together, INO80 is emerging as a major regulator of the meiotic transcription program by mediating poised chromatin establishment through SUZ12 binding.
2021-12-21 | GSE179577 | GEO
Project description:INO80 is the catalytic subunit of the multi-subunit INO80-chromatin remodeling complex that has been implicated in DNA replication, repair, and transcription regulation. Ino80-deficiency in murine spermatocytes (Ino80cKO) results in pachytene arrest of spermatocytes, due to incomplete synapsis and aberrant DNA double-strand break repair (DSBR) that leads to apoptosis. We explored the mechanism by which INO80 mediates meiotic progression. RNA-seq on Ino80cKO spermatocytes revealed major changes in transcription, indicating that an aberrant transcription program arises upon INO80 depletion. In Ino80WTspermatocytes, genome-wide analysis showed that INO80-binding sites were mostly promoter proximal and necessary for the regulation of spermatogenic gene expression, primarily of premeiotic and meiotic genes. Further, most of the genes poised for activity, as well as those genes that are active, shared INO80 binding. In Ino80cKO spermatocytes, most poised genes demonstrated de-repression due to reduced H3K27me3 enrichment, and in turn showed increased expression levels. INO80 interacts with the core PRC2 complex member SUZ12 and promotes its recruitment. Further, INO80 mediates H2A.Z incorporation at the poised promoters, which was reduced in Ino80cKO spermatocytes. Taken together, INO80 is emerging as a major regulator of the meiotic transcription program by mediating poised chromatin establishment through SUZ12 binding.
2021-12-21 | GSE179580 | GEO
Project description:INO80 is the catalytic subunit of the multi-subunit INO80-chromatin remodeling complex that has been implicated in DNA replication, repair, and transcription regulation. Ino80-deficiency in murine spermatocytes (Ino80cKO) results in pachytene arrest of spermatocytes, due to incomplete synapsis and aberrant DNA double-strand break repair (DSBR) that leads to apoptosis. We explored the mechanism by which INO80 mediates meiotic progression. RNA-seq on Ino80cKO spermatocytes revealed major changes in transcription, indicating that an aberrant transcription program arises upon INO80 depletion. In Ino80WTspermatocytes, genome-wide analysis showed that INO80-binding sites were mostly promoter proximal and necessary for the regulation of spermatogenic gene expression, primarily of premeiotic and meiotic genes. Further, most of the genes poised for activity, as well as those genes that are active, shared INO80 binding. In Ino80cKO spermatocytes, most poised genes demonstrated de-repression due to reduced H3K27me3 enrichment, and in turn showed increased expression levels. INO80 interacts with the core PRC2 complex member SUZ12 and promotes its recruitment. Further, INO80 mediates H2A.Z incorporation at the poised promoters, which was reduced in Ino80cKO spermatocytes. Taken together, INO80 is emerging as a major regulator of the meiotic transcription program by mediating poised chromatin establishment through SUZ12 binding.
2021-12-21 | GSE179583 | GEO
Project description:Background: Chromatin remodeling complexes facilitate the access of enzymes that mediate transcription, replication or repair of DNA by modulating nucleosome position and/or composition. Ino80 is the DNA-dependent Snf2-like ATPase subunit of a complex whose nucleosome remodeling activity requires actin-related proteins, Arp4, Arp5 and Arp8, as well as two RuvB-like DNA helicase subunits. Budding yeast mutants deficient for Ino80 function are not only hypersensitive to reagents that induce DNA double strand breaks, but also to those that impair replication fork progression. Results: To understand why ino80 mutants are sensitive to agents that perturb DNA replication, we used chromatin immunoprecipitation to map the binding sites of the Ino80 chromatin remodeling complex on four budding yeast chromosomes. We found that Ino80 and Arp5 binding sites coincide with origins of DNA replication and tRNA genes. In addition, Ino80 was bound at 67% of the promoters of genes that are sensitive to ino80 mutation. When replication forks were arrested near origins in the presence of hydroxyurea (HU), the presence of the Ino80 complex at stalled forks and at unfired origins increased dramatically. Importantly, the resumption of DNA replication after release from a HU block was impaired in the absence of Ino80 activity. Mutant cells accumulated double-strand breaks as they attempted to restart replication. Consistently, ino80-deficient cells, although proficient for checkpoint activation, delay recovery from the checkpoint response. Conclusions: The Ino80 chromatin remodeling complex is enriched at stalled replication forks where it promotes the resumption of replication upon recovery from fork arrest. Keywords: ChIP-chip • The goal of the experiment Genome-wide localization of Ino80 on chromosome in Saccharomyces cerevisiae • Keywords DNA replication, Saccharomyces cerevisiae, Genome tilling array (chromosome III, IV, V, VI) • Experimental factor Distribution of Ino80 in random culture Distribution of Ino80 in G1 phase Distribution of Ino80 in early S phase • Experimental design ChIP analyses: W303 background cells expressing Myc-tagged Ino80 were used for the ChIP using anti-Myc monoclonal antibody (9E11). ChIP-chip analyses: In all cases, hybridization data for ChIP fraction was compared with WCE (whole cell extract) fraction. Saccharomyces cerevisiae affymetrix genome tiling array (SC3456a520015F for chromosome III, IV, V, VI) was used. • Quality control steps taken Confirmation of several loci by quantitative real time PCR.
2008-04-10 | E-GEOD-9420 | biostudies-arrayexpress
Project description:The mechanistics by which ATP-dependent chromatin remodelers process (epi)genetic information to generate hallmark features of chromatin are fundamental for genome regulation. Here, we advance whole-genome reconstitutions into a fully definable, recombinant approach for probing how remodelers determine nucleosome positioning. Using wild type and structure-guided mutant versions of the Saccharomyces cerevisiae 15-subunit INO80 remodeler, we show that INO80-intrinsic nucleosome positioning relies on direct DNA shape read-out. This requires especially the interplay between the INO80 nuclear actin and core modules, to a lesser extent the HMG-box Nhp10 module and not histone modifications/variants or the Rvb1/2 AAA+-ATPase activity. Extrinsically, nucleosome positioning is guided by the barrier Reb1 via Ino80 ATPase activity modulation or by mere DNA double strand breaks. Taken together, we present a defined and unbiased approach to understand remodeler-mediated nucleosome positioning and delineate how INO80 processes genomic information into nucleosome positioning.
2020-04-30 | GSE145093 | GEO
Project description:We report the high-throughput profiling of INO80 knockdown by siRNA in human kidney-2 cells (HK-2). We found that downstream target genes of INO80. This study provides novel insights into the chromatin remodeling factors regulated by INO80 in renal epithelial cells.
2023-08-23 | GSE224479 | GEO