Cell functions are based on the integrity of actin filaments. The actin cytoskeleton is typically the target but also the source of signals. Arabidopsis PRL1 (Pleiotropic Regulatory Locus 1), regulates multiple cellular processes and physiological responses. However, the precise mechanisms underlying PRL1`s multiple functions are unclear. Here, we show that PRL1 maintains actin integrity and concomitant cellular homeostasis. The cortical actin cytoskeleton was de-polymerized in the prl1 mutant, causing the developmental root defect. Actin depolymerization, rather than reactive oxygen species (ROS) imbalance, constituted the fundamental cause of retarded root growth in prl1. ANAC085 upregulation by, and cooperation with, actin depolymerization triggered stele cell death in prl1 roots. Differential gene expression and alternative splicing defects resulting from actin depolymerization occurred independently in prl1. Our work establishes the cause-effect relationships between actin depolymerization and downstream stress-related signals, revealing a novel function of PRL1 and enhancing the understanding of PRL`s functional mechanisms.

磷酸化是真核细胞中常见的一种翻译后修饰方式,它对生物体内多种代谢活动和细胞信号转导过程起着调控作用.植物病毒蛋白通过磷酸化和去磷酸化修饰调节蛋白质的生物活性,从而影响细胞内的生物信号传递.磷酸化修饰的植物病毒蛋白参与调控病毒的侵染、病毒RNA的合成、病毒的RNA沉默以及调控宿主基因的表达.近年来,植物病毒蛋白磷酸化的分子机制得到了广泛和深入的研究.本文总结了植物病毒蛋白磷酸化修饰的位点、磷酸化鉴定方法及其生物学功能,为磷酸化在植物和病毒相互作用中的生物学功能提供了参考.

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 (H 2 O 2 and O 2 ·– ) 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 .

Actin dynamic is critical for cell morphogenesis in plants, but the signaling mechanisms underlying its regulation are not well understood. Here we found PRL1 ( P leiotropic R egulatory L ocus1) modulates leaf pavement cell (PC) morphogenesis in Arabidopsis by maintaining the dynamic homeostasis of actin microfilaments (MF). Our previous studies indicated PC shape formation was mediated by the counteracting ROP2 and ROP6 signaling pathways that promote the organization of cortical MF and microtubules (MT), respectively. Our genetic screen for ROP6 enhancers identified prl1 alleles. Genetic analysis suggested that prl1 acted synergistically with ROP2 and ROP6 in regulation of PC morphogenesis. We further found that the activities of ROP2 and ROP6 were increased and decreased in prl1 mutants, respectively. Interestingly prl1 was found to prefer to depolymerize MF independent of ROP2 and ROP6. Stress (high salinity and low temperature) induced similar changes of ROP activities as do prl1 mutations. Together our findings provided evidence that PRL1 governed two signaling pathways that counteractively maintain actin dynamics and resultant cell morphogenesis.