Myoblast differentiation is associated with and benefits from increased autophagy
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA890311 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21898826_1.fastq.gz | Fastqsanger.gz | |||
| SRR21898826_2.fastq.gz | Fastqsanger.gz | |||
| SRR21898827_1.fastq.gz | Fastqsanger.gz | |||
| SRR21898827_2.fastq.gz | Fastqsanger.gz | |||
| SRR21898828_1.fastq.gz | Fastqsanger.gz |
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Project description:The goal of this study was to identify potentially novel mechanisms that mediate myoblast differentiation using the C2C12 cell as a myoblast model. The study started with an RNA-seq analysis to identify genes differentially expressed during myoblast differentiation. This analysis and subsequent functional analysis resulted in the identification of autophagy as one of the upregulated biological processes in differentiating myoblasts.
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Project description:Wnt/M-NM-2-catenin signaling is involved in various aspects of skeletal muscle development and regeneration. In addition, Wnt3a and M-NM-2-catenin are required for muscle-specific gene transcription in embryonic carcinoma cells and satellite-cell proliferation during adult skeletal muscle regeneration. Downstream targets of canonical Wnt signaling are cyclin D1 and c-myc. However, both target genes are suppressed during differentiation of mouse myoblast cells, C2C12. Underlying molecular mechanisms of M-NM-2-catenin signaling during myogenic differentiation remain unknown. Using C2C12 cells, we examined intracellular signaling and gene transcription during myoblast proliferation and differentiation. We confirmed that several Wnt signaling components, including Wnt9a, Sfrp2 and porcupine, were consistently upregulated in differentiating C2C12 cells. Troponin T-positive myotubes were decreased by Wnt3a overexpression, but not Wnt4. TOP/FOP reporter assays revealed that co-expression with Wnt4 reduced Wnt3a-induced luciferase activity, suggesting that Wnt4 signaling counteracted Wnt3a signaling in myoblasts. FH535, a small-molecule inhibitor of M-NM-2-catenin/Tcf complex formation, reduced basal M-NM-2-catenin in cytoplasm and decreased myoblast proliferation. K252a, a protein kinase inhibitor, increased membrane-bound M-NM-2-catenin and enhanced myoblast fusion. Treatments with K252a or Wnt4 resulted in increased cytoplasmic vesicles containing phosphorylated M-NM-2-catenin (Tyr654) during myogenic differentiation. These results suggest that various Wnt ligands control subcellular M-NM-2-catenin localization, which regulate myoblast proliferation and myotube formation. Wnt signaling via M-NM-2-catenin likely acts as a molecular switch that regulates the transition from cell proliferation to myogenic differentiation. Control cells (day 0) prior to differentiation induction with n=4; differentiated for two days with n=3; differentiated for four days with n=3.
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Project description:Wnt/β-catenin signaling is involved in various aspects of skeletal muscle development and regeneration. In addition, Wnt3a and β-catenin are required for muscle-specific gene transcription in embryonic carcinoma cells and satellite-cell proliferation during adult skeletal muscle regeneration. Downstream targets of canonical Wnt signaling are cyclin D1 and c-myc. However, both target genes are suppressed during differentiation of mouse myoblast cells, C2C12. Underlying molecular mechanisms of β-catenin signaling during myogenic differentiation remain unknown. Using C2C12 cells, we examined intracellular signaling and gene transcription during myoblast proliferation and differentiation. We confirmed that several Wnt signaling components, including Wnt9a, Sfrp2 and porcupine, were consistently upregulated in differentiating C2C12 cells. Troponin T-positive myotubes were decreased by Wnt3a overexpression, but not Wnt4. TOP/FOP reporter assays revealed that co-expression with Wnt4 reduced Wnt3a-induced luciferase activity, suggesting that Wnt4 signaling counteracted Wnt3a signaling in myoblasts. FH535, a small-molecule inhibitor of β-catenin/Tcf complex formation, reduced basal β-catenin in cytoplasm and decreased myoblast proliferation. K252a, a protein kinase inhibitor, increased membrane-bound β-catenin and enhanced myoblast fusion. Treatments with K252a or Wnt4 resulted in increased cytoplasmic vesicles containing phosphorylated β-catenin (Tyr654) during myogenic differentiation. These results suggest that various Wnt ligands control subcellular β-catenin localization, which regulate myoblast proliferation and myotube formation. Wnt signaling via β-catenin likely acts as a molecular switch that regulates the transition from cell proliferation to myogenic differentiation.
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Project description:Identification of product of proteolysis during C2C12 myoblast differentiation using subtiligase N-terminomics. Different cell populations collected during a time-course of differentiation (4 days) were used for N-terminal labeling in a forward degradomics approach (n=2). Day0 population= Myoblasts, Day1 populations= live cells and dead cells, Day4 populations= Myotubes and Reserve cells. Additionally, cleavages events generated by mouse caspase-3 at early stages of differentiation (Day 0 and 1) was evaluated using a reverse degradomics approach on myoblasts and live cells (n=2).
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Project description:Circadian rhythms regulate cell differentiation and tissue regeneration; however, their implications in tissue regeneration remain elusive. Here, we present evidence that tissue regeneration efficiency is dependent on the circadian timing of injury affliction in a mouse model of muscle injury. We found that depletion of Per1 or Per2, members of the core circadian regulators in vertebrates, impaired mouse muscle regeneration and myoblast differentiation. Both Per1 and Per2 were necessary to maintain the expression level of Igf2, one of the critical regulators for myoblast differentiation, through epigenetic regulation at the Igf2 promoter and enhancer. Reflecting this, myoblast differentiation was promoted when differentiation was initiated while the level of Pers and Igf2 were high, compared with the time when their expression levels were low. Furthermore, muscle regeneration in the mouse was more efficient when chemical injury was inflicted at night when Pers were highly expressed, compared with morning injury. This study uncovers circadian timing-based control of myoblast differentiation and muscle regeneration.
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Project description:For hematopoietic stem and progenitor cells (HSPCs), hypoxia is a specific microenvironment known as the hypoxic niche. The role of hypoxia in maintaining quiescence, self-renewal and proliferation of HSPCs has been more elaborated. What remains unclear is the regulation of hypoxia on HSPC differentiation, especially on the differentiation of HSPCs into erythrocytes. In this study, we show that hypoxia evidently accelerates erythroid differentiation, and in this process effectively enhances autophagy which rapidly supplies cellular components through degradation of organelles or proteins to meet the needs of cell stress or development. In order to ascertain whether autophagy mediates the erythroid differentiation promoted by hypoxia, we analyze the perturbation of erythroid differentiation after pharmacological and genetic interference with autophagy, and address that autophagy is required for hypoxia-accelerated erythroid differentiation. Transcriptomics reveals HIF-1 and mTORC1 pathways may function as the upstream of autophagy to regulate erythroid differentiation under hypoxia. We further determine that mTORC1 signaling is suppressed by hypoxia to relieve its inhibition of autophagy. In addition, we also discover a new regulatory pattern that with the process of erythroid differentiation, mTORC1 activity gradually decreases and autophagy activity increases concomitantly. Moreover, we provide evidence that HIF-1 target gene REDD1, which inhibits mTORC1 activity, is dramatically upregulated under hypoxia. Silencing REDD1 expression activates mTORC1 signaling and impairs the enhanced autophagy and the accelerated erythroid differentiation under hypoxia. Together, our study reveals that hypoxia is conductive to accelerating erythroid differentiation, in which autophagy induced by the HIF-1/REDD1/mTORC1 pathway plays a pivotal role.
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Project description:Expression profiling of C2C12 myoblast cells treated with ethanol during differentiation. Ethanol inhibits C2C12 differentiation. Results provide insight into signaling pathways altered by ethanol during differentiation. When C2C12 cells reached 70% confluence in growth medium containing 20% FBS, culture medium was changed to differentiation medium containing 2% horse serum with and without 100mM ethanol. Samples were harvested from day zero (just prior to differentiation) as well as days 1, 2 and 3 following onset of differentiation with and without alcohol treatment. RNA was isolated using the Qiagen RNA mini-kit.
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