Journal
JOURNAL OF CELL BIOLOGY
Volume 174, Issue 3, Pages 403-413Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200601102
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Funding
- NIAMS NIH HHS [R01 AR048884, AR-48884, R01 AR052730, AR-052730, R01 AR051372, AR-051372, AR-047315] Funding Source: Medline
- NIGMS NIH HHS [T32-GM08367, T32 GM008367] Funding Source: Medline
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Myoblast fusion is critical for the formation, growth, and maintenance of skeletal muscle. The initial formation of nascent myotubes requires myoblast - myoblast fusion, but further growth involves myoblast - myotube fusion. We demonstrate that the mannose receptor (MR), a type I transmembrane protein, is required for myoblast - myotube fusion. Mannose receptor ( MR) - null myotubes were small in size and contained a decreased myonuclear number both in vitro and in vivo. We hypothesized that this defect may arise from a possible role of MR in cell migration. Time-lapse microscopy revealed that MR-null myoblasts migrated with decreased velocity during myotube growth and were unable to migrate in a directed manner up a chemoattractant gradient. Furthermore, collagen uptake was impaired in MR-null myoblasts, suggesting a role in extracellular matrix remodeling during cell motility. These data identify a novel function for MR during skeletal muscle growth and suggest that myoblast motility may be a key aspect of regulating myotube growth.
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