Programmed Cell Death in Plant Immunity: Cellular Reorganization, Signaling, and Cell Cycle Dependence in Cultured Cells as a Model System

Abstract

Plants have evolved various means for controlled and organized cell destruction, known as programmed cell death (PCD). PCD is a crucial event in plant immunity against microbial infection that prevents the spread of pathogens. Plants lack homologs of most apoptosis-related genes in animals and have evolved specific mechanisms for PCD. Cryptogein-triggered defense responses and PCD in tobacco BY-2 cells are a useful simple model system to monitor cellular events in which most plant defense responses can be mimicked. Recent live cell imaging techniques have revealed the dynamic features and significant roles of the cytoskeleton, such as actin microfilaments and microtubules, as well as the vacuole, an organelle occupying most of the cell volume, during defense responses and PCD. Both the production of reactive oxygen species (ROS) by NADPH oxidase and its temporal pattern have been suggested to play a crucial role in triggering and regulating PCD. Prior to the induction of defense responses and PCD, cell cycle arrest is induced either at G1 or G2 phase. In turn, defense signaling and responses including PCD are dependent on cell cycle phases and are only induced following cell cycle arrest. Here, we overview the dynamic reorganization of the cellular architecture, signaling events, and interrelationship between the cell cycle and innate immunity/PCD.