Stimulus-specific accumulation of second messengers like reactive oxygen species (ROS) and Ca(2+) are central to many signaling and regulation processes in plants. However, mechanisms that govern the reciprocal interrelation of Ca(2+) and ROS signaling are only beginning to emerge. NADPH oxidases of the respiratory burst oxidase homolog (RBOH) family are critical components contributing to the generation of ROS while Calcineurin B-like (CBL) Ca(2+) sensor proteins together with their interacting kinases (CIPKs) have been shown to function in many Ca(2+)- signaling processes. In this study, we identify direct functional interactions between both signaling systems. We report that the CBL-interacting protein kinase CIPK26 specifically interacts with the N-terminal domain of RBOHF in yeast two-hybrid analyses and with the full-length RBOHF protein in plant cells. In addition, CIPK26 phosphorylates RBOHF in vitro and co-expression of either CBL1 or CBL9 with CIPK26 strongly enhances ROS production by RBOHF in HEK293T cells. Together, these findings identify a direct interconnection between CBL-CIPK-mediated Ca(2+) signaling and ROS signaling in plants and provide evidence for a synergistic activation of the NADPH oxidase RBOHF by direct Ca(2+)-binding to its EF-hands and Ca(2+)-induced phosphorylation by CBL1/9-CIPK26 complexes.
Highlights d Iron-regulated and calcium-dependent protein kinase CIPK11 interacts with FIT d CIPK11 and calcium sensors CBL1/9 promote FIT-dependent Fe deficiency responses d FIT is phosphorylated in plants, and CIPK11 phosphorylates FIT at Ser272 d Mutation at Ser272 modulates FIT activity, affecting seed iron content
Soil composition largely defines the living conditions of plants and represents one of their most relevant, dynamic and complex environmental cues. The effective concentrations of many either tolerated or essential ions and compounds in the soil usually differ from the optimum that would be most suitable for plants. In this regard, salinity - caused by excess of NaCl - represents a widespread adverse growth condition but also shortage of ions like K+, NO3- and Fe2+ restrains plant growth. During the past years many components and mechanisms that function in the sensing and establishment of ion homeostasis have been identified and characterized. Here, we reflect on recent insights that extended our understanding of components and mechanisms, which govern and fine-tune plant salt stress tolerance and ion homeostasis. We put special emphasis on mechanisms that allow for interconnection of the salt overly sensitivity pathway with plant development and discuss newly emerging functions of Ca2+ signaling in salinity tolerance. Moreover, we review and discuss accumulating evidence for a central and unifying role of Ca2+ signaling and Ca2+ dependent protein phosphorylation in regulating sensing, uptake, transport and storage processes of various ions. Finally, based on this cross-field inventory, we deduce emerging concepts and arising questions for future research.
In plants, potassium (K ) homeostasis is tightly regulated and established against a concentration gradient to the environment. Despite the identification of Ca -regulated kinases as modulators of K channels, the immediate signaling and adaptation mechanisms of plants to low-K conditions are only partially understood. To assess the occurrence and role of Ca signals in Arabidopsis thaliana roots, we employed ratiometric analyses of Ca dynamics in plants expressing the Ca reporter YC3.6 in combination with patch-clamp analyses of root cells and two-electrode voltage clamp (TEVC) analyses in Xenopus laevis oocytes. K deficiency triggers two successive and distinct Ca signals in roots exhibiting spatial and temporal specificity. A transient primary Ca signature arose within 1 min in the postmeristematic stelar tissue of the elongation zone, while a secondary Ca response occurred after several hours as sustained Ca elevation in defined tissues of the elongation and root hair differentiation zones. Patch-clamp and TEVC analyses revealed Ca dependence of the activation of the K channel AKT1 by the CBL1-CIPK23 Ca sensor-kinase complex. Together, these findings identify a critical role of cell group-specific Ca signaling in low K responses and indicate an essential and direct role of Ca signals for AKT1 K channel activation in roots.
NON-PHOTOTROPIC HYPOCOTYL 3 (NPH3) is a key component of the auxin-dependent plant phototropic growth response. We report that NPH3 directly binds polyacidic phospholipids, required for plasma membrane association in darkness. We further demonstrate that blue light induces an immediate phosphorylation of a C-terminal 14-3-3 binding motif in NPH3. Subsequent association of 14-3-3 proteins is causal for the light-induced release of NPH3 from the membrane and accompanied by NPH3 dephosphorylation. In the cytosol, NPH3 dynamically transitions into membraneless condensate-like structures. The dephosphorylated state of the 14-3-3 binding site and NPH3 membrane recruitment are recoverable in darkness. NPH3 variants that constitutively localize either to the membrane or to condensates are non-functional, revealing a fundamental role of the 14-3-3 mediated dynamic change in NPH3 localization for auxin-dependent phototropism. This regulatory mechanism might be of general nature, given that several members of the NPH3-like family interact with 14-3-3 via a C-terminal motif.
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