Computational modeling reveals that Abl signaling tunes actin networks between connected and fragmented states primarily through changes to the level of dendricity

Abstract

Abl signaling, a crucial pathway for neural patterning, steers growth cones primarily by altering actin dynamics. Biochemical and genetic evidence shows that Abl modifies cytoskeletal organization by promoting the actin brancher, Arp2/3, and by inhibiting the processive linear polymerase, Enabled. Despite knowledge of both the multi-micron changes to the actin network and the molecular perturbations downstream of Abl, an emergent mechanism that explains how the downstream effectors alter network architecture is incomplete.