No abstract

Plant morphogenesis relies on the accurate positioning of the partition (cell plate) between dividing cells during cytokinesis. The cell plate is synthetized by a specialized structure called the phragmoplast, which consists of microtubules, actin filaments, membrane compartments and associated proteins. The phragmoplast forms between daughter nuclei during the transition from anaphase to telophase. As cells are commonly larger than the originally formed phragmoplast, the construction of the cell plate requires phragmoplast expansion. This expansion depends on microtubule polymerization at the phragmoplast forefront (leading zone) and loss at the back (lagging zone). Leading and lagging zones sandwich the 'transition' zone. A population of stable microtubules in the transition zone facilitates transport of building materials to the midzone where the cell plate assembly takes place. Whereas microtubules undergo dynamic instability in all zones, the overall balance appears to be shifted towards depolymerization in the lagging zone. Polymerization of microtubules behind the lagging zone has not been reported to date, suggesting that microtubule loss there is irreversible. In this Review, we discuss: (1) the regulation of microtubule dynamics in the phragmoplast zones during expansion; (2) mechanisms of the midzone establishment and initiation of cell plate biogenesis; and (3) signaling in the phragmoplast.

Calcium and reactive oxygen species (ROS) are two of the earliest second messengers in response to environmental stresses in plants. The rise and sequestration of these messengers in the cytosol and apoplast are formed by various channels, transporters, and enzymes that are required for proper defense responses. It remains unclear how calcium and ROS signals regulate each other during pattern-triggered immunity (PTI). In the present study, we examined the effects of perturbing one signal on the other in Arabidopsis leaves upon the addition of flg22, a well-studied microbe-associated molecular pattern (MAMP). To this end, a variety of pharmacological agents were used to suppress either calcium or ROS signaling. Our data suggest that cytosolic calcium elevation is required to initiate and regulate apoplastic ROS production generated by respiratory burst oxidase homologs (RBOHs). In contrast, ROS has no effect on the initiation of the calcium signal, but is required for forming a sufficient amplitude of the calcium signal. This finding using pharmacological agents is corroborated by the result of using a genetic double mutant, rbohd rbohf. Our study provides an insight into the mutual interplay of calcium and ROS signals during the MAMP-induced PTI response in plants.

A quantitative and robust bioassay to assess plant defense response is important for studies of disease resistance and also for the early identification of disease during pre- or non-symptomatic phases. An increase in extracellular pH is known to be an early defense response in plants. In this study, we demonstrate extracellular alkalinization as a defense response in potatoes. Using potato suspension cell cultures, we observed an alkalinization response against various pathogen- and plant-derived elicitors in a dose- and time-dependent manner. We also assessed the defense response against a variety of potato pathogens, such as protists (Phytophthora infestans and Spongospora subterranea) and fungi (Verticillium dahliae and Colletotrichum coccodes). Our results show that extracellular pH increases within 30 min in proportion to the number of pathogen spores added. Consistently with the alkalinization effect, the higher transcription level of several defense-related genes and production of reactive oxygen species was observed. Our results demonstrate that the alkalinization response is an effective marker to study early stages of defense response in potatoes.

No abstract