Wnt7a Activates the Planar Cell Polarity Pathway to Drive the Symmetric Expansion of Satellite Stem Cells

Grand, Fabien Le; Jones, Andrew; Seale, Vanessa; Scimè, Anthony; Rudnicki, Michael A.

doi:10.1016/j.stem.2009.03.013

Cited by 440 publications

(559 citation statements)

References 45 publications

Supporting

Mentioning

521

Contrasting

Unclassified

Order By: Relevance

“…Another critical question is whether the Wnt-independent functions of b-catenin and/or b-catenin-independent functions of Wnt signaling contribute to the complexities of stem cell regulation. Superimposed on these issues is the increasing evidence that noncanonical Wnt pathways can powerfully influence stem cell behavior ranging from the roles of PCP in symmetric cell divisions of muscle satellite stem cells (Le Grand et al 2009) to roles for noncanonical Wnt signaling in the hematopoietic stem cell niche as well as its aging counterparts (Sugimura et al 2012;Florian et al 2013). Whether these pathways compete for shared components such as the Dvl proteins and whether there are feedback circuitries that affect the regulation of these Wnt pathways will no doubt provide plenty of fuel for future investigations.…”

Section: Concluding Statementsmentioning

confidence: 99%

Wnt some lose some: transcriptional governance of stem cells by Wnt/β-catenin signaling

2014

View full text Add to dashboard Cite

In mammals, Wnt/b-catenin signaling features prominently in stem cells and cancers, but how and for what purposes have been matters of much debate. In this review, we summarize our current knowledge of Wnt/b-catenin signaling and its downstream transcriptional regulators in normal and malignant stem cells. We centered this review largely on three types of stem cells-embryonic stem cells, hair follicle stem cells, and intestinal epithelial stem cells-in which the roles of Wnt/b-catenin have been extensively studied. Using these models, we unravel how many controversial issues surrounding Wnt signaling have been resolved by dissecting the diversity of its downstream circuitry and effectors, often leading to opposite outcomes of Wnt/b-catenin-mediated regulation and differences rooted in stage-and context-dependent effects.

show abstract

Section: Concluding Statementsmentioning

confidence: 99%

Wnt some lose some: transcriptional governance of stem cells by Wnt/β-catenin signaling

2014

View full text Add to dashboard Cite

show abstract

“…They are known to function at distinct phases of regeneration: with Notch functioning at the early phase to promote satellite cell activation and proliferation and Wnt at the later phase to promote myoblast differentiation [24][25][26]. In addition to Notch and Wnt, members of the interleukin-6 (IL-6) family of cytokines are also implicated in muscle differentiation and regeneration.…”

Section: Introductionmentioning

confidence: 99%

Oncostatin M inhibits myoblast differentiation and regulates muscle regeneration

Xiao

Wang

et al. 2010

Cell Res

View full text Add to dashboard Cite

Oncostatin M (OSM) is a cytokine of the interleukin-6 family and plays important roles during inflammation. However, its roles in myoblast differentiation and muscle regeneration remain unexplored. We show here that OSM potently inhibited myoblast differentiation mainly by activating the JAK1/STAT1/STAT3 pathway. OSM downregulated myocyte enhancer-binding factor 2A (MEF2A), upregulated the expression of Id1 and Id2, and inhibited the transcriptional activity of MyoD and MEF2. In addition, OSM also enhanced the expression of STAT3 and OSM receptor, which constituted a positive feedback loop to further amplify OSM-induced signaling. Moreover, we found that STAT1 physically associated with MEF2 and repressed its transcriptional activity, which could account for the OSM-mediated repression of MEF2. Although undetectable in normal muscles in vivo, OSM was rapidly induced on muscle injury and then promptly downregulated just before the majority of myoblasts differentiate. Prolonged expression of OSM in muscles compromised the regeneration process without affecting myoblast proliferation, suggesting that OSM functions to prevent proliferating myoblasts from premature differentiation during the early phase of muscle regeneration.

show abstract

“…4 WNT (wingless-type MMTV integration site family) signaling factors are known to regulate both the maintenance of muscle satellite cells (MSCs), and their ability to differentiate into myofibers. [5][6][7] Conversely, both dystrophic and aged skeletal muscle display activated WNT signaling resulting in increased muscle fibrosis. 8 In DMD, a similar dysregulation of the transcriptional-level WNT signaling components has been reported.…”

mentioning

confidence: 99%

MicroRNA-199a is induced in dystrophic muscle and affects WNT signaling, cell proliferation, and myogenic differentiation

et al. 2013

View full text Add to dashboard Cite

In patients with Duchenne muscular dystrophy (DMD), the absence of a functional dystrophin protein results in sarcolemmal instability, abnormal calcium signaling, cardiomyopathy, and skeletal muscle degeneration. Using the dystrophin-deficient sapje zebrafish model, we have identified microRNAs (miRNAs) that, in comparison to our previous findings in human DMD muscle biopsies, are uniquely dysregulated in dystrophic muscle across vertebrate species. MiR-199a-5p is dysregulated in dystrophindeficient zebrafish, mdx 5cv mice, and human muscle biopsies. MiR-199a-5p mature miRNA sequences are transcribed from stem loop precursor miRNAs that are found within the introns of the dynamin-2 and dynamin-3 loci. The miR-199a-2 stem loop precursor transcript that gives rise to the miR-199a-5p mature transcript was found to be elevated in human dystrophic muscle. The levels of expression of miR-199a-5p are regulated in a serum response factor (SRF)-dependent manner along with myocardin-related transcription factors. Inhibition of SRF-signaling reduces miR-199a-5p transcript levels during myogenic differentiation. Manipulation of miR-199a-5p expression in human primary myoblasts and myotubes resulted in dramatic changes in cellular size, proliferation, and differentiation. MiR-199a-5p targets several myogenic cell proliferation and differentiation regulatory factors within the WNT signaling pathway, including FZD4, JAG1, and WNT2. Overexpression of miR-199a-5p in the muscles of transgenic zebrafish resulted in abnormal myofiber disruption and sarcolemmal membrane detachment, pericardial edema, and lethality. Together, these studies identify miR-199a-5p as a potential regulator of myogenesis through suppression of WNT-signaling factors that act to balance myogenic cell proliferation and differentiation.

show abstract

Wnt7a Activates the Planar Cell Polarity Pathway to Drive the Symmetric Expansion of Satellite Stem Cells

Cited by 440 publications

References 45 publications

Wnt some lose some: transcriptional governance of stem cells by Wnt/β-catenin signaling

Wnt some lose some: transcriptional governance of stem cells by Wnt/β-catenin signaling

Oncostatin M inhibits myoblast differentiation and regulates muscle regeneration

MicroRNA-199a is induced in dystrophic muscle and affects WNT signaling, cell proliferation, and myogenic differentiation

Contact Info

Product

Resources

About