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Myosin-Specific Adaptations of In vitro Fluorescence Microscopy-Based Motility Assays
Published on: February 4, 2021
Myosin IIA deficient cells migrate efficiently despite reduced traction forces at cell periphery
Melissa H Jorrisch1, Wenting Shih, Soichiro Yamada
1Department of Biomedical Engineering, University of California Davis , Davis, CA 95616 , USA.
Biology Open
|April 26, 2013
Summary
Myosin II isoforms A and B play distinct roles in cell migration. Myosin IIA-deficient cells migrate faster with less force, demonstrating cellular adaptability in motility.
Area of Science:
- Cell biology
- Biophysics
Background:
- Cell motility is crucial for development and disease.
- Migrating cells typically exert traction forces on the extracellular matrix.
- The role of specific myosin II isoforms in force generation during migration is unclear.
Purpose of the Study:
- To investigate the individual roles of myosin IIA and IIB in cell migration and traction force generation.
- To determine how myosin II isoform depletion affects cellular structures involved in motility.
Main Methods:
- Utilized micron-sized pillar arrays as force sensors.
- Employed short hairpin RNA (shRNA) to specifically deplete myosin IIA and IIB.
- Analyzed cell migration speed and traction force generation.
Main Results:
- Myosin IIA and IIB localized to the leading and trailing edges, respectively.
- Myosin IIA depletion resulted in loss of stress fibers and focal adhesions.
- Myosin IIA-deficient cells migrated faster but generated less traction force compared to wild-type or myosin IIB-deficient cells.
Conclusions:
- Myosin IIA is involved in generating traction forces at the cell periphery.
- Cells can migrate efficiently with reduced peripheral traction forces, highlighting adaptive mechanisms.
- Myosin IIB plays a role in maintaining cellular structures during migration.
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