Journal
MOLECULAR BIOLOGY OF THE CELL
Volume 25, Issue 12, Pages 1845-1853Publisher
AMER SOC CELL BIOLOGY
DOI: 10.1091/mbc.E13-08-0450
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Funding
- National Science Foundation [DMR-0844115]
- Institute for Complex Adaptive Matter Branches Cost Sharing Fund
- Burroughs Wellcome Fund Career Awards at the Scientific Interface
- American Asthma Foundation
- Packard Foundation
- University of Chicago Materials Research Science and Engineering Center
- Division Of Materials Research
- Direct For Mathematical & Physical Scien [0844115] Funding Source: National Science Foundation
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Myosin II motors embedded within the actin cortex generate contractile forces to modulate cell shape in essential behaviors, including polarization, migration, and division. In sarcomeres, myosin II-mediated sliding of antiparallel F-actin is tightly coupled to myofibril contraction. By contrast, cortical F-actin is highly disordered in polarity, orientation, and length. How the disordered nature of the actin cortex affects actin and myosin movements and resultant contraction is unknown. Here we reconstitute a model cortex in vitro to monitor the relative movements of actin and myosin under conditions that promote or abrogate network contraction. In weakly contractile networks, myosin can translocate large distances across stationary F-actin. By contrast, the extent of relative actomyosin sliding is attenuated during contraction. Thus actomyosin sliding efficiently drives contraction in actomyosin networks despite the high degree of disorder. These results are consistent with the nominal degree of relative actomyosin movement observed in actomyosin assemblies in nonmuscle cells.
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