Niche Cadherins Control the Quiescence-to-Activation Transition in Muscle Stem Cells
Open accessAbstract
Many adult stem cells display prolonged quiescence, promoted by cues from their niche. Upon tissue damage, a coordinated transition to the activated state is required because non-physiological breaks in quiescence often lead to stem cell depletion and impaired regeneration. Here, we identify cadherin-mediated adhesion and signaling between muscle stem cells (satellite cells [SCs]) and their myofiber niche as a mechanism that orchestrates the quiescence-to-activation transition. Conditional removal of N-cadherin and M-cadherin in mice leads to a break in SC quiescence, with long-term expansion of a regeneration-proficient SC pool. These SCs have an incomplete disruption of the myofiber-SC adhesive junction and maintain niche residence and cell polarity, yet show properties of SCs in a state of transition from quiescence toward full activation. Among these is nuclear localization of β-catenin, which is necessary for this phenotype. Injury-induced perturbation of niche adhesive junctions is therefore a likely first step in the quiescence-to-activation transition.
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Diminishment of the SC pool is not observed when SCs-SC niche molecular interactions are interrupted in muscles lacking Wnt4, N-, and M-cadherins or syndecan-3.
“Interestingly, diminishment of the SC pool is not observed when SCs-SC niche molecular interactions are interrupted in muscles lacking Wnt4, N-, and M-cadherins or syndecan-323,39,40.”
From In vivo partial reprogramming of myofibers promotes muscle regeneration by remodeling the stem cell niche (2021) · cites this paper as [39]
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- Authors
- Goel, A. J., Rieder, M.-K., Arnold, H.-H., Radice, G. L., & Krauss, R. S.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- Technische Universität Braunschweig (DE)
- Thomas Jefferson University (US)
- Corresponding author
- Krauss, Robert S.
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2017-11
- Volume
- 21
- Issue
- 8
- Pages
- 2236-2250
- ISSN
- 2211-1247 (ISSN-L)
- PMC
- PMC5702939
- OpenAlex
- W2770114366
- Cited by
- 146
- References
- 67
- Citations by year
- 2026: 17 · 2025: 16 · 2024: 27 · 2023: 11 · 2022: 19 · 2021: 20 · 2020: 19 · 2019: 14 · 2018: 3
- FWCI
- 4.02
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- The Medicine Forum (submittedVersion, cc-by-nc-nd)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Institutes of Health (AR070231, AR046207)
- Deutsche Forschungsgemeinschaft
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Keywords
- muscle stem cells, satellite cells, N-cadherin, M-cadherin, cadherin-mediated adhesion, β-catenin nuclear localization, muscle regeneration, tissue damage, stem cell depletion, cell polarity
- MeSH terms
- Animals, Cell Division, Regeneration, Stem Cells, Signal Transduction, Cadherins, Cell Polarity, Muscle, Skeletal, Satellite Cells, Skeletal Muscle, Cell Proliferation, Mice
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