Adverse variations of abiotic environmental cues that deviate from an optimal range impose stresses to plants. Abiotic stresses severely impede plant physiology and development. Consequently, such stresses dramatically reduce crop yield and negatively impact on ecosystem stability and composition. Physical components of abiotic stresses can be, for example, suboptimal temperature and osmotic perturbations, while representative chemical facets of abiotic stresses can be toxic ions or suboptimal nutrient availability. The sheer complexity of abiotic stresses causes a multitude of diverse components and mechanisms for their sensing and signal transduction. Ca 2+ , as a versatile second messenger, plays multifaceted roles in almost all abiotic stress responses in that, for a certain abiotic stress, Ca 2+ is not only reciprocally connected with its perception, but also multifunctionally ensures subsequent signal transduction. Here, we will focus on salt/osmotic stress and responses to altered nutrient availability as model cases to detail novel insights into the identity of components that link stress perception to Ca 2+ signal formation as well as on new insights into mechanisms of Ca 2+ signal implementation. Finally, we will deduce emerging conceptual consequences of these novel insights and outline arising avenues of future research on the role of Ca 2+ signaling in abiotic stress responses in plants.

No abstract

No abstract

Soil salinity adversely affects plant growth, crop yield and the composition of ecosystems. Salinity stress impacts plants by combined effects of Na toxicity and osmotic perturbation. Plants have evolved elaborate mechanisms to counteract the detrimental consequences of salinity. Here we reflect on recent advances in our understanding of plant salt tolerance mechanisms. We discuss the embedding of the salt tolerance-mediating SOS pathway in plant hormonal and developmental adaptation. Moreover, we review newly accumulating evidence indicating a crucial role of a transpiration-dependent salinity tolerance pathway, that is centred around the function of the NADPH oxidase RBOHF and its role in endodermal and Casparian strip differentiation. Together, these data suggest a unifying and coordinating role for Ca signalling in combating salinity stress at the cellular and organismal level.

Homeostasis of the essential micronutrient manganese (Mn) is crucially determined through availability and uptake efficiency in all organisms. Mn deficiency of plants especially occurs in alkaline and calcareous soils, seriously restricting crop yield. However, the mechanisms underlying the sensing and signaling of Mn availability and conferring regulation of Mn uptake await elucidation. Here, we uncover that Mn depletion triggers spatiotemporally defined long-lasting Ca 2+ oscillations in Arabidopsis roots. These Ca 2+ signals initiate in individual cells, expand, and intensify intercellularly to transform into higher-order multicellular oscillations. Furthermore, through an interaction screen we identified the Ca 2+ -dependent protein kinases CPK21 and CPK23 as Ca 2+ signal-decoding components that bring about translation of these signals into regulation of uptake activity of the high-affinity Mn transporter natural resistance associated macrophage proteins 1 (NRAMP1). Accordingly, a cpk21 / 23 double mutant displays impaired growth and root development under Mn-limiting conditions, while kinase overexpression confers enhanced tolerance to low Mn supply to plants. In addition, we define Thr498 phosphorylation within NRAMP1 as a pivot mechanistically determining NRAMP1 activity, as revealed by biochemical assays and complementation of yeast Mn uptake and Arabidopsis nramp1 mutants. Collectively, these findings delineate the Ca 2+ -CPK21/23-NRAMP1 axis as key for mounting plant Mn homeostasis.

No abstract

Soil salinity impairs plant growth reducing crop productivity. Toxic accumulation of sodium ions is counteracted by the Salt Overly Sensitive (SOS) pathway for Na + extrusion, comprising the Na + transporter SOS1, the kinase SOS2, and SOS3 as one of several Calcineurin-B-like (CBL) Ca 2+ sensors. Here, we report that the receptor-like kinase GSO1/SGN3 activates SOS2, independently of SOS3 binding, by physical interaction and phosphorylation at Thr16. Loss of GSO1 function renders plants salt sensitive and GSO1 is both sufficient and required for activating the SOS2-SOS1 module in yeast and in planta. Salt stress causes the accumulation of GSO1 in two specific and spatially defined areas of the root tip: in the endodermis section undergoing Casparian strip (CS) formation, where it reinforces the CIF-GSO1-SGN1 axis for CS barrier formation; and in the meristem, where it creates the GSO1-SOS2-SOS1 axis for Na + detoxification. Thus, GSO1 simultaneously prevents Na + both from diffusing into the vasculature, and from poisoning unprotected stem cells in the meristem. By protecting the meristem, receptor-like kinase-conferred activation of the SOS2-SOS1 module allows root growth to be maintained in adverse environments.

Increasing soil salinity is a major problem in global crop production. The detrimental effect of saline soils on plant growth results from ionic toxicity of the Na+ ion in combination...