RT Journal Article SR Electronic T1 Rac1 is a downstream effector of PKCα in structural synaptic plasticity JF bioRxiv FD Cold Spring Harbor Laboratory SP 750372 DO 10.1101/750372 A1 Xun Tu A1 Ryohei Yasuda A1 Lesley A Colgan YR 2019 UL http://biorxiv.org/content/early/2019/08/29/750372.abstract AB Structural and functional plasticity of dendritic spines is the basis of animal learning. The calcium-dependent protein kinase C isoform, PKCα, has been suggested to be critical for this actin-dependent plasticity. However, mechanisms linking PKCα and structural plasticity of spines are unknown. Here, we examine the spatiotemporal activation of actin regulators, including small GTPases Rac1, Cdc42 and Ras, in the presence or absence of PKCα during single-spine structural plasticity. Removal of PKCα expression in the postsynapse attenuated Rac1 activation during structural plasticity without affecting Ras or Cdc42 activity. Moreover, disruption of a PDZ binding domain within PKCα led to impaired Rac1 activation and deficits in structural spine remodeling. These results demonstrate that PKCα positively regulates the activation of Rac1 during structural plasticity.