Pleiotropic Regulatory Locus1 maintains actin microfilament integrity and concomitant cellular homeostasis facilitating root development in Arabidopsis

Cell functions are based on integrity of actin filaments. The Actin cytoskeleton is typically the target but also the source of signals. An evolutionarily conserved WD-40 protein PRL1 (Pleiotropic Regulatory Locus1) in Arabidopsis was investigated with multilayer functions in development, innate immunity, alternative splicing activation, transcription regulation, genome maintenance, ubiquitination-based protein turnover et al., but the underlying mechanisms are undefined. Here, we show PRL1 maintains actin integrity and concomitant cellular homeostasis. To explore causes for developmental root defect, we found depolymerization of cortical actin cytoskeleton and ROS imbalance in prl1 mutant. Further, we revealed that actin de-polymerization was the fundamental cause and dominant to ROS imbalance (H2O2 and O2{middle dot}-) for retarded root of prl1; NAC085 was up-regulated by and cooperated with actin depolymerization to mediate to stele cell death. Moreover, we revealed stress-related differentially expressed genes and alternative splicing defects were mutually independent and were responses to actin depolymerization in prl1. Our work ravels out cause-effect relationships between actin configuration and downstream hierarchical signals and explores underlying mechanism for functions of PRL1.