Myosin 1c and myosin IIB serve opposing roles in lamellipodial dynamics of the neuronal growth cone

Abstract

The myosin family of motor proteins is implicated in mediating actin-based growth cone motility, but the roles of many myosins remain unclear. We previously implicated myosin 1c (Mlc; formerly myosin 1β) in the retention of lamellipodia (Wang et al., 1996). Here we address the role of myosin II (MII) in chick dorsal root ganglion neuronal growth cone motility and the contribution of M1c and Mil to retrograde F-actin flow using chromophore-assisted laser inactivation (CALI). CALI of Mil reduced neurite outgrowth and growth cone area by 25%, suggesting a role for Mil in lamellipodial expansion. Micro-CALI of MII caused a rapid reduction in local lamellipodial protrusion in growth cones with no effects on filopodial dynamics. This is opposite to micro-CALI of M1c, which caused an increase in lamellipodial protrusion. We used fiduciary beads (Forscher et al., 1992) to observe retrograde F-actin flow during the acute loss of M1c or MII. Micro-CALI of M1c reduced retrograde bead flow by 76%, whereas micro-CALI of Mil or the MIIB isoform did not. Thus, Mlc and MIIB serve opposite and nonredundant roles in regulating lamellipodial dynamics, and Mlc activity is specifically required for retrograde F-actin flow.