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Symmetric neural progenitor divisions require chromatin-mediated homologous recombination DNA repair by Ino80

ABSTRACT: Symmetric neural progenitor divisions require chromatin-mediated homologous recombination DNA repair by Ino80

PROVIDER: PRJNA641343 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12075290_1.fastq.gz	Fastqsanger.gz
	SRR12075290_2.fastq.gz	Fastqsanger.gz
	SRR12075291_1.fastq.gz	Fastqsanger.gz
	SRR12075291_2.fastq.gz	Fastqsanger.gz
	SRR9641420.fastq.gz	Fastqsanger.gz

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

2020-06-23 | GSE153061 | GEO

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

2020-06-25 | GSE133799 | GEO

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

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

| PRJNA641347 | ENA

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

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

| PRJNA552556 | ENA

Symmetric neural progenitor divisions require chromatin-mediated homologous recombination DNA repair by Ino80

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-06-23 | GSE153062 | GEO

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

Project description: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.

2017-05-14 | GSE95801 | GEO

RNA methylation maintains hematopoietic stem cell identity and symmetric commitment

Project description:Stem cells balance cellular fates through asymmetric and symmetric divisions in order to self-renew or to generate downstream progenitors. Symmetric commitment divisions in stem cells are required for rapid regeneration during tissue damage and stress. The control of symmetric commitment remains poorly defined. N6-methyladenosine (m6A), the most abundant posttranscriptional mRNA modification controls cellular states and its abundance is dysregulated in cancer. Here we show that mRNA methylation controls symmetric commitment and cell identity of hematopoietic stem cells (HSCs). Using single-cell RNA sequencing (scRNA-seq) in combination with transcriptomic profiling of HSPCs (hematopoietic stem and progenitor cells) from control and m6A methyltransferase Mettl3 conditional knockout mice, we found that m6A-deficient HSC fail to symmetrically differentiate. Dividing HSCs are expanded and are blocked in an intermediate state that molecularly and functionally resembles multipotent progenitors. Mechanistically, RNA methylation controls Myc mRNA abundance in differentiating HSCs. Importantly, we identified MYC as a new marker for HSC asymmetric and symmetric commitment. Furthermore, forced expression of MYC rescued m6A’s requirement for engraftment indicating its importance in the early stage of HSC cellular fate. Overall our results indicate that RNA methylation is critical for normal blood homeostasis and may provide a general mechanism for how stem cells regulate differentiation fate choice.

2019-07-25 | GSE132357 | GEO

Regulation of cellular heterogeneity and rates of symmetric and asymmetric divisions in triple-negative breast cancer

Project description:Regulation of cellular heterogeneity and rates of symmetric and asymmetric divisions in triple-negative breast cancer

| PRJNA328149 | ENA

Aberrant activation of p53/p66Shc-mInsc axis increases asymmetric divisions and attenuates proliferation of aged mammary stem cells.

Project description:Mammary gland aging is due to aberrant activation of p66Shc, which induces p53/p44 signaling, leading to failure of symmetric divisions, decreased proliferation and reduced regenerative potential of MaSCs. Age-related changes in mammary epithelial cells derived from C57BL/6J WT and p66Shc knockedout mice cultured as stem cell-enriched mammospheres.

2022-12-21 | GSE201253 | GEO

Knockdown of Ino80 complex subunits Actr5, Ies6, and Ino80 in RD cells

Project description:INO80 complex is an ATPase-dependent chormatin remodeling complex, which regulates various DNA metabolic processes such as DNA replication and repair. Additionally, INO80 complex also contributes to the regulation of gene expression in sterss response and development. In order to investigate the function of INO80 complex in rhabdomyosarcoma, we examined the knockdown of subunits of INO80 complex Actr5, Ies6, and Ino80 in human rhabdomyosarcoma RD cells. As a result, it was found that INO80 complex is involved in the sarcomagenicity and the disregulation of myogenic properties of rhabdomyosarcoma cells.

2022-04-01 | GSE169681 | GEO

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