The transition from G0 to GAlert is regulated by GLI3 processing by the primary cilia
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA605180 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11035156.fastq.gz | Fastqsanger.gz | |||
| SRR11035157.fastq.gz | Fastqsanger.gz | |||
| SRR11035158.fastq.gz | Fastqsanger.gz | |||
| SRR11035159.fastq.gz | Fastqsanger.gz | |||
| SRR11035160.fastq.gz | Fastqsanger.gz |
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Project description:Satellite stem cells are required for the growth, maintenance, and regeneration of skeletal muscle. Quiescent satellite stem cells possess a primary cilium, a structure that regulates the processing of the GLI-family of transcription factors. We find that GLI3, specifically, plays a critical role in satellite cell activation. Strikingly, primary cilia-mediated processing of GLI3, independent of canonical Hedgehog signaling, is required to maintain satellite cells in a G0 dormant state, as satellite cells lacking GLI3 enter GAlert in absence of injury. Furthermore, GLI3 depletion or inhibition of its processing stimulates symmetrical division in satellite cells and expansion of the stem cell pool. As a result, satellite cells lacking GLI3 display rapid cell-cycle entry, increased proliferation and augmented self-renewal, and markedly enhanced long-term regenerative capacity. Therefore, our results reveal an essential role for primary cilia processing of GLI3 in regulating muscle stem cell activation.
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2009-05-22 | E-MEXP-2188 | biostudies-arrayexpress
Project description:Background: Whereas cilia damage and reduced cilia beat frequency have been implicated as causative of reduced mucociliary clearance in smokers, theoretically mucociliary clearance could also be affected by cilia length. Based on models of mucociliary clearance predicting cilia length must exceed the 6 -7 μm airway surface fluid depth to generate force in the mucus layer, we hypothesized cilia height may be decreased in airway epithelium of normal smokers compared to nonsmokers. Methodology/Principal Findings: Cilia length in normal nonsmokers and smokers was evaluated in aldehyde-fixed, paraffin-embedded endobronchial biopsies, and air-dried and hydrated samples brushed from human airway epithelium via fiberoptic bronchoscopy. In 28 endobronchial biopsies, healthy smoker cilia length was reduced 15% compared to nonsmokers (p<0.05). In 47 air-dried samples of airway epithelial cells, smoker cilia length was reduced 13% compared to nonsmokers (p<0.0001). Analysis of the length of individual, detached cilia in 17 samples, smoker cilia length was reduced 9% compared to nonsmokers (p<0.05). Finally, in 16 fully hydrated, unfixed samples, smoker cilia length was reduced 7% compared to nonsmokers (p<0.05). Conclusions/significance: Models predict that a reduction in cilia length would reduce mucociliary clearance, suggesting that smoking-associated shorter airway epithelial cilia plays a significant role in the pathogenesis of smoking-induced lung disease.
2012-12-13 | E-GEOD-16696 | biostudies-arrayexpress
Project description:NIH3T3 in the middle of G0 to G1 transion consists of the cells which is still staying G0 phase and the cells which enters G1. Monitoring the expressions of p27 and Cdt1 enables to distinguish these two; p27+/Cdt1+ cells as the cells in G0 phase and p27-Cdt1+ cells as G1 phase We sorted p27+Cdt1+ (G0) NIH3T3 cells and p27-Cdt1+ (G1) NIH3T3 cells in the middle of G0-G1 transition, 5 hours after serum addition following the serum addition using mVenus-p27K- and mCherry-hCdt1(30/120) . We compared the expression profiles of these NIH3T3 cells in G0 and G1 phases and identified the genes upregulated in G0 or G1 phases.
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Project description:Purpose: This study seeks to determine whether GLI3 is required to recruit the SMARCC1 complex to GLI enhancers in the limb. Methods: To determine if Gli3 is required to recruit SMARCC1 to its anhancers, we performed differential chromatin binding to compare SMARCC1 binding in control and Gli3 mutants. We performed Cut&Run for SMARCC1 binding on individually genotyped E11.5 (40-43s) anterior forelimb pairs from control (Gli3+/+; 3 replicates) and Gli3 mutant (Gli3-/-; 4 replicates) embryos. Results: We found that there is no major difference in SMARCC1 binding in Gli3-mutants compared to controls.
2024-02-03 | GSE224508 | GEO
Project description:To investigate GLI3 TF targets during organoid fate decisions, we performed Cut&Tag of GLI3 binding
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Project description:NIH3T3 in the middle of G0 to G1 transion consists of the cells which is still staying G0 phase and the cells which enters G1. Monitoring the expressions of p27 and Cdt1 enables to distinguish these two; p27+/Cdt1+ cells as the cells in G0 phase and p27-Cdt1+ cells as G1 phase We sorted p27+Cdt1+ (G0) NIH3T3 cells and p27-Cdt1+ (G1) NIH3T3 cells in the middle of G0-G1 transition, 5 hours after serum addition following the serum addition using mVenus-p27K- and mCherry-hCdt1(30/120) . We compared the expression profiles of these NIH3T3 cells in G0 and G1 phases and identified the genes upregulated in G0 or G1 phases. The p27+Cdt1+ (G0) NIH3T3 cells and p27-Cdt1+ (G1) NIH3T3 cells were sorted by FACS for RNA extraction and hybridization on Affymetrix microarrays.
2014-02-21 | E-GEOD-46511 | biostudies-arrayexpress
Project description:Aim: To determine the major protein kinase pathways altered upon serum- or LPA-induced cilia disassembly Primary cilia are dynamic structures which must disassemble for a cell to go through mitosis and re-assemble in G0 to transduce essential signals. Also, in non-cycling cells (such as renal epithelial cells), there is evidence to suggest that deregulated cilia disassembly is of critical importance, for example in instances with an excess of a cilia disassembly stimuli (such as Aurora kinase A expression and activation, a key disassembly factor) which is associated with ciliopathy phenotypes and a net loss of ciliated cells. Serum, growth factor or lysophosphatidic acid (LPA) stimulation of ciliated cells are well established experimental paradigms for the induction of cilia disassembly. The signalling network activated by these stimuli that culminates in cilia disassembly is complex and poorly understood. Studies have generally focused on a single or small group of proteins of interest to define their roles in cilia disassembly and the key pathways and kinases activated upon serum stimulation to induce cilia disassembly have not been defined. Moreover, to the best of our knowledge an unbiased analysis of the major pathways activated during cilia disassembly has not been performed. Ciliated hTERT-RPE1 cells were treated with 10% serum or 2 M LPA for 15’ or 2 h to initiate cilia disassembly + pan-class I PI3K inhibitor GDC-0941, followed by label-free phosphoproteomics.
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