ArticleThe Journal of biological chemistry2011
Phospholipase D regulates myogenic differentiation through the activation of both mTORC1 and mTORC2 complexes.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Transcriptome analysis reveals the long intergenic noncoding RNAs contributed to skeletal muscle differences between Yorkshire and Tibetan pig.Scientific reports · 2021Article
- Mitochondrial ROS-derived PTEN oxidation activates PI3K pathway for mTOR-induced myogenic autophagy.Cell death and differentiation · 2018Article
- Phospholipase D in TCR-Mediated Signaling and T Cell Activation.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- AnMolecular and cellular biology · 2017Article
- Differentiation capacities of skeletal muscle satellite cells in Lantang and Landrace piglets.Oncotarget · 2017Article
- Article
- Heterogeneous nuclear ribonucleoprotein M associates with mTORC2 and regulates muscle differentiation.Scientific reports · 2017Article
- From Nutrient to MicroRNA: a Novel Insight into Cell Signaling Involved in Skeletal Muscle Development and Disease.International journal of biological sciences · 2016Review
- Phospholipase D1 facilitates second-phase myoblast fusion and skeletal muscle regeneration.Molecular biology of the cell · 2015Article
- Role of the mTORC1 complex in satellite cell activation by RNA-induced mitochondrial restoration: dual control of cyclin D1 through microRNAs.Molecular and cellular biology · 2014Article
- New roles for Smad signaling and phosphatidic acid in the regulation of skeletal muscle mass.F1000prime reports · 2014Review
- Phospholipase D regulates the size of skeletal muscle cells through the activation of mTOR signaling.Cell communication and signaling : CCS · 2013Article
- IKK-β mediates hydrogen peroxide induced cell death through p85 S6K1.Cell death and differentiation · 2013Article
- Mammalian target of rapamycin (mTOR) signaling network in skeletal myogenesis.The Journal of biological chemistry · 2012Review
- TNF-α- and tumor-induced skeletal muscle atrophy involves sphingolipid metabolism.Skeletal muscle · 2012Article
- Rapamycin passes the torch: a new generation of mTOR inhibitors.Nature reviews. Drug discovery · 2011Review
- Raptor and Rheb negatively regulate skeletal myogenesis through suppression of insulin receptor substrate 1 (IRS1).The Journal of biological chemistry · 2011Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
How phospholipase D (PLD) is involved in myogenesis remains unclear. At the onset of myogenic differentiation of L6 cells induced by the PLD agonist vasopressin in the absence of serum, mTORC1 complex was rapidly activated, as reflected by phosphorylation of S6 kinase1 (S6K1). Both the long (p85) and short (p70) S6K1 isoforms were phosphorylated in a PLD1-dependent way. Short rapamycin treatment specifically inhibiting mTORC1 suppressed p70 but not p85 phosphorylation, suggesting that p85 might be directly activated by phosphatidic acid. Vasopressin stimulation also induced phosphorylation of Akt on Ser-473 through PLD1-dependent activation of mTORC2 complex. In this model of myogenesis, mTORC2 had a positive role mostly unrelated to Akt activation, whereas mTORC1 had a negative role, associated with S6K1-induced Rictor phosphorylation. The PLD requirement for differentiation can thus be attributed to its ability to trigger via mTORC2 activation the phosphorylation of an effector that could be PKCα. Moreover, PLD is involved in a counter-regulation loop expected to limit the response. This study thus brings new insights in the intricate way PLD and mTOR cooperate to control myogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.