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Rbfox2-dependent alternative splicing of Numb regulates Notch signaling during muscle stem cell activation II

ABSTRACT: Satellite cells (SCs), or muscle stem cells, are the resident somatic stem cells responsible for skeletal muscle regeneration. Most SCs remain quiescent in resting adult muscles but can activate rapidly upon receiving a stimulus. While alternative splicing has been reported to play important role in stem cells , its role in the activation process of SCs remains elusive. We identified Numb as one of the genes that display rapid splicing change during SC activation. To investigate the role of Numb splicing during satellite cell activation, we use morpholino to inhibit the inculstion of Numb exon 6 on early activated SCs and performed RNA-seq to profile the transcriptome changes upon Numb splicing change.

ORGANISM(S): Mus musculus

PROVIDER: GSE290586 | GEO | 2025/12/30

REPOSITORIES: GEO

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Rbfox2-dependent alternative splicing of Numb regulates Notch signaling during muscle stem cell activation

Project description:Satellite cells (SCs), or muscle stem cells, are the resident somatic stem cells responsible for skeletal muscle regeneration. Most SCs remain quiescent in resting adult muscles but can activate rapidly upon receiving a stimulus. While Rbfox2 has been reported to play an essential role in regulating myoblast differentiation, its role in the activation process of SCs remains elusive. To investigate the role of Rbfox2 during satellite cell activation, we freshly isolated satellite cells from Rbfox2 conditional knockout mice and performed RNA-seq to profile the transcriptome changes upon Rbfox2 knockout.

2025-12-30 | GSE263621 | GEO

Effects on mRNA levels of a Numb and Numb-like conditional knockout in skeletal muscle fibers

Project description:We investigated the gene expression changes resulting from loss of Numb from skeletal muscle fibers using a conditional, inducible knockout of Numb and its close homolog Numb-like (NumbL) bulk RNA-sequencing.

2022-02-16 | GSE167390 | GEO

3 days injured in vivo ASCs proteome

Project description:Muscle Stem Cells or satellite cells (SCs) are required for muscle regeneration. In resting muscles, SCs are kept in quiescence. After injury, SCs undergo rapid activation, proliferation and differentiation to repair damaged muscles. The transcriptome alteration during SC activation is well characterized. While transcriptome is not exactly represent proteome because of post-transcriptional regulations such as miRNA induced gene silencing. However, little is known about SC proteome. We obtained in vivo activated SCs (ASCs) from 3 days post injured muscles for high resolution mass spectrometry Bruker timsTOF Pro. Compared with QSC proteome,, we identified the pathways that are differentially expressed between them.

2021-11-04 | PXD023656 | Pride

Mouse Muscle Stem Cell Proteome during Activation and CPEB1 Dependent Proteome in Mouse Muscle Stem Cell

Project description:Muscle Stem Cells or satellite cells (SCs) are required for muscle regeneration. In resting muscles, SCs are kept in quiescence. After injury, SCs undergo rapid activation, proliferation and differentiation to repair damaged muscles. The transcriptome alteration during SC activation is well characterized. While transcriptome is not exactly represent proteome because of post-transcriptional regulations such as miRNA induced gene silencing. However, little is known about SC proteome. We obtained quisecent SCs (QSCs) and freshly isolated SCs (fiSCs, early activated SCs) and activated SCs (ASCs) for high resolution mass spectrometry Bruker timsTOF Pro. Thus, we uncovered the QSC proteome. By comparison of QSC proteome to fiuSCs proteome or ASCs proteome, we identified the pathways that are differentially expressed between them. Forthermore, we characterized a translational regulator CPEB1 reprogrammed translation landscape for SC activation.

2021-11-05 | PXD018865 | Pride

Loss of NUMB drives aggressive bladder cancer via a RHOA/ROCK/YAP signaling axis.

Project description:We have discovered a previously uncharacterized tumor suppressor function of Numb in the homeostasis of the normal bladder mucosa. Targeted ablation of Numb in the basal layer of the urothelium drives spontaneous bladder tumorigenesis, driving progression from preneoplastic to preinvasive and overtly invasive tumors, and accelerates tumorigenesis in the presence of oncogenic insults. Using 3D-Matrigel organoid cultures to recapitulate bladder tumorigenesis in vitro, we found that Numb deficiency enhances the proliferative and invasive potential of both mouse and human bladder cancer cells. Integrative transcriptomic and functional analyses revealed that downregulation of the canonical Hippo pathway, resulting in enhanced YAP transcriptional activity, underlies the biological aggressiveness of Numb-deficient bladder cancer. These molecular events are dependent on the activation of RhoA/ROCK signaling subsequent to Numb loss. Thus, a dysfunctional Numb–RhoA/ROCK–Hippo/YAP regulatory network is at play in aggressive Numb-deficient bladder cancers, opening avenues for the development of targeted therapies. Furthermore, retrospective cohort studies revealed that a Numb-deficient status correlates with worse overall survival in post-cystectomy muscle-invasive bladder cancer (MIBC) patients and increased risk of progression to MIBC in non-muscle-invasive bladder cancer (NMIBC) patients. The Numb-deficient status was associated with a 27-gene prognostic signature that has the potential to identify high-risk NMIBC patients who are eligible for targeted RhoA/ROCK/YAP therapies.

2024-10-11 | GSE256272 | GEO

Regulation of NUMB alternative splicing by RBM5, RBM6 and RBM10 controls cancer cell proliferation

Project description:RBM5, a regulator of alternative splicing of apoptotic genes, and its close homologues, RBM6 and RBM10, are RNA binding proteins frequently deleted or mutated in lung cancer. We report that RBM5/6 and RBM10 antagonistically regulate the proliferative capacity of cancer cells and display distinct positional effects in alternative splicing regulation. We identify the Notch pathway regulator NUMB as a key target of these factors in the control of cell proliferation. NUMB alternative splicing, which is frequently altered in lung cancer, can regulate colony and xenograft tumor formation and its modulation recapitulates or antagonizes the effects of RBM5, 6 and 10 in cell colony formation. RBM10 mutations identified in lung cancer cells disrupt NUMB splicing regulation to promote cell growth. Our results reveal a key genetic circuit in the control of cancer cell proliferation.

2013-12-20 | GSE47431 | GEO

Numb variant specific transcriptome analysis

Project description:Numb has 4 known variants and we are reporting two novel Numb variants, Numb5 and Numb6 in this study. The metastaticability variations between the numb variants were evaulated through the transcriptome.

2011-05-09 | GSE29137 | GEO

Regulation of NUMB alternative splicing by RBM5, RBM6 and RBM10 controls cancer cell proliferation (CLIP-Seq)

2013-12-20 | GSE48066 | GEO

Epigenetic determinants of muscle stem cell quiescence and chronological aging

Project description:Skeletal muscle is a post-mitotic tissue that exhibits an extremely low turnover in the absence of disease or injury. At the same time, muscle possesses remarkable regenerative capacity mediated by satellite cells (SCs) that reside in close association with individual myofibers, underneath the fiber’s basal lamina. Consistent with the low turnover of the muscle, SCs in adult animals are mitotically quiescent and therefore provide an excellent model to study stem cell quiescence. As an organism grows older, the resident stem cells are exposed to a deteriorating environment and experience chronological aging. In stem cells with high turnover, the effects of chronological aging are superimposed upon the effects of the replicative aging that results from DNA replication and cell division. On the contrary, SCs experience minimal replicative aging due to their low turnover. They are thus a good model to study the consequence of chronological aging of quiescent stem cells. We performed microarray analysis of quiescent and activated SCs from both young and aged mice to understand the global gene expression profile underlying stem cell properties such as quiecence and self-renewal, and to understand how the transcriptome of a quiescent stem cell pouplation changes with age. VCAM+/CD31-/CD45-/Sca1- quiescent satellite cells (QSCs) were isolated by FACS from hindlimb muscle of uninjured 2-3- or 22-24-month old mice. Activated satellite cells (ASCs) were isolated from hindlimb muscles of BaCl2-injured mice of the same age 36, 60 and 84 hours after injury using the same cell surface marker combination. YFP-expressing cells were isolated from 2-3-month old Pax7CreER/+; ROSA26eYFP/+ mice in which satellite cells are labeled geneticall by YFP expression. Total RNA was extracted from cells with the Trizol reagent according to manufacturer's instructions. RNA was then processed and assayed with Affymetrix Mouse Gene 1.0 ST arrays.

2013-05-23 | E-GEOD-47177 | biostudies-arrayexpress

Epigenetic determinants of muscle stem cell quiescence and chronological aging (ChIP-seq)

Project description:Skeletal muscle is a post-mitotic tissue that exhibits an extremely low turnover in the absence of disease or injury. At the same time, muscle possesses remarkable regenerative capacity mediated by satellite cells (SCs) that reside in close association with individual myofibers, underneath the fiberM-bM-^@M-^Ys basal lamina. Consistent with the low turnover of the muscle, SCs in adult animals are mitotically quiescent and therefore provide an excellent model to study stem cell quiescence. As an organism grows older, the resident stem cells are exposed to a deteriorating environment and experience chronological aging. In stem cells with high turnover, the effects of chronological aging are superimposed upon the effects of the replicative aging that results from DNA replication and cell division. On the contrary, SCs experience minimal replicative aging due to their low turnover. They are thus a good model to study the consequence of chronological aging of quiescent stem cells. We have developed an isolation protocol to selectively enrich SCs by FACS from adult mice and applied the ChIP-seq technology to obtain H3K4me3, H3K27me3 and H3K36me3 from quiescent and activated SCs from young mice and from quiescent SCs from old mice. Our analysis aims to understand the chromatin features underlying stem cell properties such as quiecence and lineage-potency, and to understand how the chromatin structure of a quiescent stem cell pouplation changes with age. VCAM+/CD31-/CD45-/Sca1- quiescent satellite cells (QSCs) were isolated by FACS from hindlimb muscle of uninjured 2-3- or 22-24-month old mice and processed for ChIP-seq.

2013-08-13 | E-GEOD-47362 | biostudies-arrayexpress

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