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Hematopoietic stem cell niche generation and maintenance are distinguishable by an epitranscriptomic program

ABSTRACT: Hematopoietic stem cell niche generation and maintenance are distinguishable by an epitranscriptomic program

PROVIDER: PRJNA896631 | ENA |

REPOSITORIES: ENA

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Hematopoietic stem cell niche generation and maintenance are distinguishable by an epitranscriptomic program

Project description:Hematopoietic stem cell niche generation and maintenance are distinguishable by an epitranscriptomic program

| PRJNA896638 | ENA

Hematopoietic stem cell niche generation and maintenance are distinguishable by an epitranscriptomic program

Project description:Hematopoietic stem cell niche generation and maintenance are distinguishable by an epitranscriptomic program

| PRJNA896637 | ENA

Hematopoietic stem cell niche generation and maintenance are distinguishable by an epitranscriptomic program

Project description:The niche is typically considered as a pre-established structure sustaining stem cells. Therefore, the regulation of its formation remains largely unexplored. It is unknown whether distinct molecular mechanisms control the establishment versus maintenance of a stem cell niche. To address this, we compared perinatal with adult bone marrow mesenchymal stromal cells (MSCs), a key component of the hematopoietic stem cell (HSC) niche. MSCs exhibited an enrichment in genes mediating m6A mRNA methylation regulation at the perinatal stage and downregulated the expression of Mettl3, the m6A methyltransferase, shortly after birth. Deletion of Mettl3 from developing MSCs led to excessive osteogenic differentiation and a severe HSC niche formation defect, which was rescued by deletion of Klf2, a target of m6A. In contrast, deletion of Mettl3 from MSCs postnatally did not affect HSC niche or hematopoiesis. Stem cell niche generation and maintenance thus depend on divergent molecular mechanisms, which may be exploited for regenerative medicine.

2024-04-23 | GSE217055 | GEO

Hematopoietic stem cell niche generation and maintenance are distinguishable by an epitranscriptomic program

2024-04-23 | GSE217056 | GEO

Hematopoietic stem cell niche generation and maintenance are distinguishable by an epitranscriptomic program

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

2024-04-23 | GSE217057 | GEO

Epitranscriptomic regulation of cortical neural stem cell maintenance via Mettl8-dependent mitochondrial tRNA m3C modification

Project description:Increasing evidence implicates critical roles of various epitranscriptomic RNA modifications in different biological processes. Methyltransferase METTL8 installs 3-methylcytosine modification of mitochondrial tRNAs in vitro, however, its role in intact biological systems is completely unknown. Here we show that Mettl8 is localized in the mitochondria and installs m3C in mitochondrial tRNASer(UCN)/Thr in mouse embryonic cortical neural stem cells. At molecular and cellular levels, Mettl8 deletion in cortical neural stem cells leads to reduced mitochondrial protein translation and attenuated respiration activity. At the functional level, conditional Mettl8 deletion in mice results in impaired embryonic cortical neural stem cell maintenance in vivo, which can be rescued by pharmacologically enhancing mitochondrial functions. Similarly, METTL8 regulates mitochondrial protein expression and neural stem cell maintenance in human forebrain cortical organoids. Together, our study reveals a conserved epitranscriptomic mechanism of Mettl8 and mitochondrial tRNA m3C modification in maintaining embryonic cortical neural stem cells in mice and humans.

2023-01-12 | GSE214445 | GEO

Muscle stem cell niche localization, quiescence, and maintenance are cadherin-dependent but separable functions

Project description:Adhesion between stem cells and their niche promotes stable niche localization and provides signaling information to sustain properties such as quiescence. Skeletal muscle stem cells (MuSCs) are localized between an adjacent myofiber and an enwrapping basal lamina. The most abundant cadherin in MuSCs, M-cadherin, is dispensable for MuSC function, whereas N-cadherin is required to prevent MuSCs from breaking quiescence in the absence of injury. Loss of both cadherins exacerbates this phenotype, yet the MuSCs remain in the niche and maintain regenerative function. These findings raise the possibility that cadherins are dispensable for anchorage of MuSCs to their niche. To address this question, we conditionally removed from MuSCs b- and g-catenin and, separately, aE- and aT-catenin, factors essential for cadherin-dependent adhesion. Catenin-deficient MuSCs break quiescence similarly to N-/M-cadherin-deficient MuSCs, but exit the niche, and are depleted via a single fate: precocious differentiation, reentry to the niche, and fusion to myofibers. These findings indicate that separable, cadherin-dependent functions are required in MuSCs for niche localization, quiescence, and stem cell maintenance.

2024-03-07 | GSE244181 | GEO

A soft stromal niche promotes hematopoietic stem cell maintenance and rejuvenation

Project description:A soft stromal niche promotes hematopoietic stem cell maintenance and rejuvenation

| PRJNA763603 | ENA

LIM domain binding protein 1 regulates a transcriptional program essential for hematopoietic stem cell maintenance

Project description:We used ChIP-Seq to map Ldb1, Scl and Gata2 binding sites in mouse hematopoietic progenitor cells (HPCs). Together with functional studies using conventional and conditional Ldb1 deficient mouse models and bioinformatics analysis, we systematically determined a transcriptional program controlled by Ldb1 complexes in HSC maintenance. To evaluate the role of Ldb1 in hematopoietic stem cell maintenance.

2011-01-04 | E-GEOD-26031 | biostudies-arrayexpress

Epitranscriptomic regulation of cortical neural stem cell maintenance via Mettl8-dependent mitochondrial tRNA m3C modification

Project description:Epitranscriptomic regulation of cortical neural stem cell maintenance via Mettl8-dependent mitochondrial tRNA m3C modification

| PRJNA885431 | ENA

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