Arabidopsis NAP1 is essential for Arp2/3-dependent trichome morphogenesis.

Abstract

The dynamic nature of the eukaryotic actin cytoskeleton is essential for the locomotion of animal cells and the morphogenesis of plant and fungal cells. The F-actin nucleating/branching activity of the Arp2/3 complex is a key function for all of these processes. The SCAR/WAVE family represents a group of Arp2/3 activators that are associated with lamellipodia formation [1 and 2]. A protein complex of PIR121, NAP1, ABI, and HSPC300 is required for SCAR regulation by cell signaling pathways [3], but the exact nature of this interaction is controversial and represents a continually evolving model [4]. The mechanism originally proposed was of a SCAR trans repressing complex supported by evidence from in vitro experiments [3]. This model was reinforced by genetic studies in the Drosophila central nervous system [5] and Dictyostelium [6], where the knockout of certain SCAR-complex components leads to excessive SCAR-mediated actin polymerization. Conflicting data have steadily accumulated from animal tissue culture experiments suggesting that the complex activates rather than represses in vivo SCAR activity [7, 8 and 9]. Recent biochemical evidence supports the SCAR-complex activator model [9]. Here, we show that genetic observations in Arabidopsis are compatible with an activation model and provide one potential mechanism for the regulation of the newly identified Arabidopsis Arp2/3 complex.