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BMP4 and BMP6 stimulation of adult mouse muscle stem cells activates the Notch signaling pathway

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE306430 | GEO | 2025/08/25

REPOSITORIES: GEO

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BMP4 and BMP6 stimulation of adult mouse muscle stem cells activates the Notch signaling pathway [array]

Project description:Muscle stem cell (MuSC) activation, proliferation, self-renewal, and differentiation are tightly regulated processes that enable muscle development and regeneration without exhaustion of the stem cell pool. BMP signaling keeps MuSCs in a proliferative state and prevents their differentiation. We investigated the effect of bone morphogenetic protein 4 and 6 (BMP4 and BMP6) on transcriptional regulation and intracellular signaling of adult murine MuSCs using RNA-sequencing, RNA expression arrays, pathway-specific qPCR arrays, and Cleavage Under Targets and Tagmentation (CUT&Tag), which identifies the binding sites of transcription factors and the presence of specific histone marks with high spatial resolution. Freshly isolated MuSCs were grown for 42 to 72 hours, kept serum deprived for 6 hours, and then stimulated with BMP4/6. BMP4/6 addition resulted in a rapid increase in Inhibitor of DNA binding 1 (Id1)-expression, a typical BMP target gene, which peaked after one hour. As expected, stimulation with BMP4/6 resulted in a significant increase in transcription of BMP target genes such as Smad7, Nog, Id1, Klf10, and Lif, but also a strong increase in transcription of Notch pathway genes such as Hes1, Lfng, and Hey1. We showed that the important BMP pathway effectors SMAD4 and pSMAD1/5/9 bind to the promoters of these Notch targets. Our results suggest that the rapid expression of genes encoding Notch signaling components is due to direct regulation by BMP signaling.

2023-10-01 | GSE127798 | GEO

BMP4 and BMP6 stimulation of adult mouse muscle stem cells activates the Notch signaling pathway [CUT&Tag]

2025-09-17 | GSE305745 | GEO

BMP4 and BMP6 stimulation of adult mouse muscle stem cells activates the Notch signaling pathway [RNA-seq I]

2023-10-01 | GSE159594 | GEO

BMP4 and BMP6 stimulation of adult mouse muscle stem cells activates the Notch signaling pathway [RNA-Seq II]

2025-09-17 | GSE305746 | GEO

BMP4 and BMP6 stimulation of adult mouse muscle stem cells activates the Notch signaling pathway

Project description:BMP4 and BMP6 stimulation of adult mouse muscle stem cells activates the Notch signaling pathway

| PRJNA1310614 | ENA

BMP4 and BMP6 stimulation of adult mouse muscle stem cells activates the Notch signaling pathway [array]

Project description:BMP4 and BMP6 stimulation of adult mouse muscle stem cells activates the Notch signaling pathway [array]

| PRJNA525422 | ENA

BMP4 and BMP6 stimulation of adult mouse muscle stem cells activates the Notch signaling pathway [CUT&Tag]

Project description:BMP4 and BMP6 stimulation of adult mouse muscle stem cells activates the Notch signaling pathway [CUT&Tag]

| PRJNA1307544 | ENA

BMP4 and BMP6 stimulation of adult mouse muscle stem cells activates the Notch signaling pathway [RNA-seq I]

Project description:BMP4 and BMP6 stimulation of adult mouse muscle stem cells activates the Notch signaling pathway [RNA-seq I]

| PRJNA669835 | ENA

BMP4 and BMP6 stimulation of adult mouse muscle stem cells activates the Notch signaling pathway [RNA-Seq II]

Project description:BMP4 and BMP6 stimulation of adult mouse muscle stem cells activates the Notch signaling pathway [RNA-Seq II]

| PRJNA1307542 | ENA

Notch signaling is necessary to maintain quiescence in adult muscle stem cells.

Project description:Satellite cells (SCs) are myogenic stem cells found in skeletal muscle that function to repair tissue damaged by injury or disease. SCs are quiescent at rest, although the signaling pathways required to maintain quiescence are unknown. Using a transgenic Notch reporter mouse and quantitative reverse-transcription polymerase chain reaction analysis of Notch target genes, we determined that Notch signaling is active in quiescent SCs. SC-specific deletion of recombining binding protein-J? (RBP-J?), a nuclear factor required for Notch signaling, resulted in the depletion of the SC pool and muscles that lacked any ability to regenerate in response to injury. SC depletion was not due to apoptosis. Rather, RBP-J?-deficient SCs spontaneously activate, fail to self-renew, and undergo terminal differentiation. Intriguingly, most of the cells differentiate without first dividing. They then fuse with adjacent myofibers, leading to the gradual disappearance of SCs from the muscle. These results demonstrate the requirement of Notch signaling for the maintenance of the quiescent state and for muscle stem cell homeostasis by the regulation of self-renewal and differentiation, processes that are all critical for normal postnatal myogenesis.

| S-EPMC3384696 | biostudies-literature

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