期刊
JOURNAL OF CELL BIOLOGY
卷 197, 期 7, 页码 939-956出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201111052
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资金
- National Institutes of Health [RO1-NS28695, RO1-NS051786, GM-026338]
- Yale Medical Scientists Training Program [TG-T32GM07205]
- Nikon Partners-in-Research Program
The Arp2/3 complex nucleates actin filaments to generate networks at the leading edge of motile cells. Nonmuscle myosin II produces contractile forces involved in driving actin network translocation. We inhibited the Arp2/3 complex and/or myosin II with small molecules to investigate their respective functions in neuronal growth cone actin dynamics. Inhibition of the Arp2/3 complex with CK666 reduced barbed end actin assembly site density at the leading edge, disrupted actin veils, and resulted in veil retraction. Strikingly, retrograde actin flow rates increased with Arp2/3 complex inhibition; however, when myosin II activity was blocked, Arp2/3 complex inhibition now resulted in slowing of retrograde actin flow and veils no longer retracted. Retrograde flow rate increases induced by Arp2/3 complex inhibition were independent of Rho kinase activity. These results provide evidence that, although the Arp2/3 complex and myosin II are spatially segregated, actin networks assembled by the Arp2/3 complex can restrict myosin II-dependent contractility with consequent effects on growth cone motility.
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