Endoplasmic reticulum-localized CCX2 is required for osmotolerance by regulating ER and cytosolic Ca2+ dynamics in Arabidopsis

Ca2+ signals in plant cells are important for adaptive responses to environmental stresses. Here, we report that the Arabidopsis CATION/Ca2+ EXCHANGER2 (CCX2), encoding a putative cation/Ca2+ exchanger that localizes to the endoplasmic reticulum (ER), is strongly induced by salt and osmotic stresses. Compared with the WT, AtCCX2 loss-of-function mutant was less tolerant to osmotic stress and displayed the most noteworthy phenotypes (less root/shoot growth) during salt stress. Conversely, AtCCX2 gain-of-function mutants were more tolerant to osmotic stress. In addition, AtCCX2 partially suppresses the Ca2+ sensitivity of K667 yeast triple mutant, characterized by Ca2+ uptake deficiency. Remarkably, Cameleon Ca2+ sensors revealed that the absence of AtCCX2 activity results in decreased cytosolic and increased ER Ca2+ concentrations in comparison with both WT and the gain-of-function mutants. This was observed in both salt and nonsalt osmotic stress conditions. It appears that AtCCX2 is directly involved in the control of Ca2+ fluxes between the ER and the cytosol, which plays a key role in the ability of plants to cope with osmotic stresses. To our knowledge, Atccx2 is unique as a plant mutant to show a measured alteration in ER Ca2+ concentrations. In this study, we identified the ER-localized AtCCX2 as a pivotal player in the regulation of ER Ca2+ dynamics that heavily influence plant growth upon salt and osmotic stress.

Understanding the Plant Immune System

Plant immunity is controlled by a complex signaling network. Here, we discuss how the complexity of the network affects our views and approaches in studying the plant immune network. We propose that the mode of plant immunity is mainly determined by how the shared signaling network is used rather than by a signaling machinery specific to each mode, that balancing the robustness of immunity and the negative effect of immunity on plant fitness is a key driver in evolution of the immune network, that comparisons of plant mutant to wild-type phenotypes may not be very effective in elucidating the underlying signaling mechanisms, and that mechanistic understanding of the network can improve our ability to predict the performance of immunity.