Journal
JOURNAL OF CELL BIOLOGY
Volume 218, Issue 7, Pages 2329-2349Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201810054
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Funding
- National Institutes of Health [R01 NS028695, R01-GM097348]
- U.S. Department of Defense Army Research Office through Multidisciplinary University Research Initiative [W911NF1410403]
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Serotonin (5-HT) is known to increase the rate of growth cone advance via cofilin-dependent increases in retrograde actin network flow and nonmuscle myosin II activity. We report that myosin II activity is regulated by PKC during 5-HT responses and that PKC activity is necessary for increases in traction force normally associated with these growth responses. 5-HT simultaneously induces cofilin-dependent decreases in actin network density and PKC-dependent increases in point contact density. These reciprocal effects facilitate increases in traction force production in domains exhibiting decreased actin network density. Interestingly, when PKC activity was up-regulated, 5-HT treatments resulted in myosin II hyperactivation accompanied by catastrophic cofilin-dependent decreases in actin filament density, sudden decreases in traction force, and neurite retraction. These results reveal a synergistic relationship between cofilin and myosin II that is spatiotemporally regulated in the growth cone via mechanocatalytic effects to modulate neurite growth.
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