Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA methylation maintains hematopoietic stem cell identity and symmetric commitment

ABSTRACT: RNA methylation maintains hematopoietic stem cell identity and symmetric commitment

PROVIDER: PRJNA547716 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR9214160.fastq.gz	Fastqsanger.gz
	SRR9214170.fastq.gz	Fastqsanger.gz
	SRR9214180.fastq.gz	Fastqsanger.gz
	SRR9214190.fastq.gz	Fastqsanger.gz
	SRR9214200_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 84

Similar Datasets

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

m<sup>6</sup>A 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. 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 hematopoietic stem cells (HSCs) 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. We identified MYC as a marker for HSC asymmetric and symmetric commitment. Overall, our results indicate that RNA methylation controls symmetric commitment and cell identity of HSCs and may provide a general mechanism for how stem cells regulate differentiation fate choice.

| S-EPMC6818972 | biostudies-literature

Symmetric self-renewal and dormancy define functional fetal liver hematopoietic stem cells at single cell resolution

Project description:Our study disclosed previously unrecognized heterogeneity in fetal liver (FL) hematopoietic stem cells (HSC), highlighting biosynthetic dormancy as a key to symmetric self-renewal of engraftable HSC and supports recent studies demonstrating distinct developmental origins for multipotent progenitors and HSC in definitive hematopoiesis.

2023-05-24 | GSE233031 | GEO

Symmetric inheritance of parental histones governs epigenome maintenance and stem cell identity

Project description:Symmetric inheritance of parental histones governs epigenome maintenance and stem cell identity

| PRJNA646113 | ENA

RACK1 maintains mouse hematopoietic stem cell quiescence

Project description:RACK1 maintains mouse hematopoietic stem cell quiescence

| PRJNA1050789 | ENA

Transcriptional plasticity, priming and commitment in hematopoietic lineages

Project description:Transcriptional plasticity, priming and commitment in hematopoietic lineages

| PRJNA451321 | ENA

MafB maintains β-cell identity under MafA-deficient condition

Project description:MafB maintains β-cell identity under MafA-deficient condition

| PRJNA824305 | ENA

Discrete regulatory modules instruct hematopoietic lineage commitment and differentiation

Project description:Discrete regulatory modules instruct hematopoietic lineage commitment and differentiation

| PRJNA759863 | ENA

Symmetric inheritance of parental histones governs epigenome maintenance and stem cell identity

Project description:Modified parental histones are segregated symmetrically to daughter DNA strands during replication and inherited through mitosis. How this may sustain the epigenome and cell identity remains unknown. Here, we show that transmission of histone-based information during replication maintains epigenome fidelity and embryonic stem cell plasticity. Asymmetric segregation of parental histones H3-H4 in MCM2-2A mutants compromised mitotic inheritance of histone modifications and globally altered the epigenome. This included widespread spurious deposition of repressive modifications, suggesting elevated epigenetic noise. Moreover, H3K9me3 loss at repeats caused de-repression and H3K27me3 redistribution across bivalent promoters correlated with misexpression of developmental genes. MCM2-2A mutation challenged dynamic transitions in cellular states across the cell cycle, enhancing naïve pluripotency and reducing lineage priming in G1. Further, developmental competence was diminished, correlating with impaired exit from pluripotency. Collectively, this argues that epigenetic inheritance of histone modifications maintains a correctly balanced and dynamic chromatin landscape able to support mammalian differentiation.

2023-06-15 | GSE154391 | GEO

Symmetric inheritance of parental histones governs epigenome maintenance and stem cell identity [RNA-seq]

Project description:Symmetric inheritance of parental histones governs epigenome maintenance and stem cell identity [RNA-seq]

| PRJNA646124 | ENA