Phosphatidylserine directly and positively regulates fusion of myoblasts into myotubes

Jeong, Jae‐Weon; Conboy, Irina M.

doi:10.1016/j.bbrc.2011.08.128

Cited by 63 publications

(52 citation statements)

References 25 publications

(21 reference statements)

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“…Studies in Drosophila have yet to reveal any molecular components that directly facilitate this step of myoblast fusion. However, studies in cultured mouse C2C12 myoblasts in vitro suggested that transient exposure of phosphatidylserine (PS) on the cell surface may play a role in myoblast fusion [49,50]. Consistent with this hypothesis, Hochreiter-Hufford et al identified a function for Brain-specific angiogenesis inhibitor 1 (BAI1), a cell surface receptor for PS, in myoblast fusion in vivo [51] (Figure 3).…”

Section: The Third Step Toward Myoblast Fusion – Destabilizing the LImentioning

confidence: 95%

Mechanisms of myoblast fusion during muscle development

Kim

Jin

Duan

et al. 2015

Current Opinion in Genetics & Development

204

172

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The development and regeneration of skeletal muscles require the fusion of mononulceated muscle cells to form multinucleated, contractile muscle fibers. Studies using a simple genetic model, Drosophila melanogaster, have discovered many evolutionarily conserved fusion-promoting factors in vivo. Recent work in zebrafish and mouse also identified several vertebrate-specific factors required for myoblast fusion. Here, we integrate progress in multiple in vivo systems and highlight conceptual advance in understanding how muscle cell membranes are brought together for fusion. We focus on the molecular machinery at the fusogenic synapse and present a three-step model to describe the molecular and cellular events leading to fusion pore formation.

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Section: The Third Step Toward Myoblast Fusion – Destabilizing the LImentioning

confidence: 95%

Mechanisms of myoblast fusion during muscle development

Kim

Jin

Duan

et al. 2015

Current Opinion in Genetics & Development

204

172

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“…2 B, Right). Mammalian skeletal muscle is formed by the proliferation, differentiation, and fusion of myogenic precursor myoblast cells into multinucleated myotubes, and PS greatly enhances this fusion event (35,36).…”

Section: Discussionmentioning

confidence: 99%

Lipidomics reveals diurnal lipid oscillations in human skeletal muscle persisting in cellular myotubes cultured in vitro

Loizides‐Mangold

Perrin

Vandereycken

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Circadian clocks play an important role in lipid homeostasis, with impact on various metabolic diseases. Due to the central role of skeletal muscle in whole-body metabolism, we aimed at studying muscle lipid profiles in a temporal manner. Moreover, it has not been shown whether lipid oscillations in peripheral tissues are driven by diurnal cycles of rest-activity and food intake or are able to persist in vitro in a cell-autonomous manner. To address this, we investigated lipid profiles over 24 h in human skeletal muscle in vivo and in primary human myotubes cultured in vitro. Glycerolipids, glycerophospholipids, and sphingolipids exhibited diurnal oscillations, suggesting a widespread circadian impact on muscle lipid metabolism. Notably, peak levels of lipid accumulation were in phase coherence with core clock gene expression in vivo and in vitro. The percentage of oscillating lipid metabolites was comparable between muscle tissue and cultured myotubes, and temporal lipid profiles correlated with transcript profiles of genes implicated in their biosynthesis. Lipids enriched in the outer leaflet of the plasma membrane oscillated in a highly coordinated manner in vivo and in vitro. Lipid metabolite oscillations were strongly attenuated upon siRNA-mediated clock disruption in human primary myotubes. Taken together, our data suggest an essential role for endogenous cell-autonomous human skeletal muscle oscillators in regulating lipid metabolism independent of external synchronizers, such as physical activity or food intake.lipid metabolism | circadian clock | human skeletal muscle | human primary myotubes | lipidomics C ircadian oscillations are daily cycles in behavior and physiology that are driven by the existence of underlying intrinsic biological clocks with near 24-h periods. This anticipatory mechanism has evolved to ensure that all aspects of behavior and physiology, including metabolic pathways, are temporally coordinated with daily cycles of rest-activity and feeding to provide the organism with an adaptive advantage (1). In mammals, circadian oscillations are driven by a master pacemaker, located in the suprachiasmatic nucleus (SCN) of the hypothalamus, which orchestrates subsidiary oscillators in peripheral organs via neuronal, endocrine, and metabolic signaling pathways (2, 3).Large-scale gene expression datasets suggest that, in mammals, the vast majority of circadian-gene expression is highly organ-specific (4-6). Key metabolic functions in peripheral organs are subject to daily oscillations, such as carbohydrate and lipid metabolism by the liver, skeletal muscle, and endocrine pancreas (7).Skeletal muscle is a major contributor of whole-body metabolism and is the main site of glucose uptake in the postprandial state (8). Therefore, perturbations in glucose sensing and metabolism in skeletal muscle are strongly associated with insulin resistance in type 2 diabetes (T2D) (9). Recent data support a fundamental role for the circadian muscle clock in the regulation of glucose uptake, with a significant re...

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“…90 Intriguingly, PS recognition is important for the formation of myotubes. 84,91,92 In vivo, expression of the well-characterized PS receptor BAI1 is required for muscle regeneration, further strengthening the link between cell death in the tissue, exposure and recognition of PS and successful tissue healing. 84 Phagocytes uphold muscle stem cell differentiation and function.…”

Section: The Predators: Macrophages Scavenge Muscle Debrismentioning

confidence: 99%