Potassium (K + ) is one of the essential nutrient elements for plant growth and development. Plants absorb K + ions from the environment via root cell K + channels and/or transporters. In this study, the Shaker K + channel Os-AKT1 was characterized for its function in K + uptake in rice (Oryza sativa) roots, and its regulation by Os-CBL1 (Calcineurin B-Like protein1) and Os-CIPK23 (CBL-Interacting Protein Kinase23) was investigated. As an inward K + channel, Os-AKT1 could carry out K + uptake and rescue the low-K + -sensitive phenotype of Arabidopsis thaliana akt1 mutant plants. Rice Os-akt1 mutant plants showed decreased K + uptake and displayed an obvious low-K + -sensitive phenotype. Disruption of Os-AKT1 significantly reduced the K + content, which resulted in inhibition of plant growth and development. Similar to the AKT1 regulation in Arabidopsis, Os-CBL1 and Os-CIPK23 were identified as the upstream regulators of Os-AKT1 in rice. The Os-CBL1-Os-CIPK23 complex could enhance Os-AKT1-mediated K + uptake. A phenotype test confirmed that Os-CIPK23 RNAi lines exhibited similar K + -deficient symptoms as the Os-akt1 mutant under low K + conditions. These findings demonstrate that Os-AKT1-mediated K + uptake in rice roots is modulated by the Os-CBL1-Os-CIPK23 complex.

Panicle size is a critical determinant of grain yield in rice () and other grain crops. During rice growth and development, spikelet abortion often occurs at either the top or the basal part of the panicle under unfavorable conditions, causing a reduction in fertile spikelet number and thus grain yield. In this study, we report the isolation and functional characterization of a panicle abortion mutant named (). exhibits degeneration of spikelets on the apical portion of panicles during late stage of panicle development. Cellular and physiological analyses revealed that the apical spikelets in the mutant undergo programmed cell death, accompanied by nuclear DNA fragmentation and accumulation of higher levels of HO and malondialdehyde. Molecular cloning revealed that harbors a mutation in, which encodes a putative aluminum-activated malate transporter (OsALMT7) localized to the plasma membrane, and is preferentially expressed in the vascular tissues of developing panicles. Consistent with a function for OsALMT7 as a malate transporter, the panicle of the mutant contained less malate than the wild type, particularly at the apical portions, and injection of malate into the panicle could alleviate the spikelet degeneration phenotype. Together, these results suggest that OsALMT7-mediated transport of malate into the apical portion of panicle is required for normal panicle development, thus highlighting a key role of malate in maintaining the sink size and grain yield in rice and probably other grain crops.

Highlights d Generation of salt-induced calcium signal requires downstream targets in Arabidopsis d AtANNEXIN4 is involved in controlling calcium transients d SOS2 phosphorylates AtANN4 under salt stress, which alters calcium signatures d A negative feedback loop fine-tunes calcium signal and optimizes plant salt response

The non-protein amino acid γ-aminobutyric acid (GABA) has been proposed to be an ancient messenger for cellular communication conserved across biological kingdoms. GABA has well-defined signalling roles in animals; however, whilst GABA accumulates in plants under stress it has not been determined if, how, where and when GABA acts as an endogenous plant signalling molecule. Here, we establish endogenous GABA as a bona fide plant signal, acting via a mechanism not found in animals. Using Arabidopsis thaliana, we show guard cell GABA production is necessary and sufficient to reduce stomatal opening and transpirational water loss, which improves water use efficiency and drought tolerance, via negative regulation of a stomatal guard cell tonoplast-localised anion transporter. We find GABA modulation of stomata occurs in multiple plants, including dicot and monocot crops. This study highlights a role for GABA metabolism in fine tuning physiology and opens alternative avenues for improving plant stress resilience.

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.

Potassium (K+) is required by plants for growth and development, and also contributes to immunity against pathogens. However, it has not been established whether pathogens modulate host K+ signaling pathways to enhance virulence and subvert host immunity. Here, we show that the effector protein AvrPiz-t from the rice blast pathogen Magnaporthe oryzae targets a K+ channel to subvert plant immunity. AvrPiz-t interacts with the rice plasma-membrane-localized K+ channel protein OsAKT1 and specifically suppresses the OsAKT1-mediated K+ currents. Genetic and phenotypic analyses show that loss of OsAKT1 leads to decreased K+ content and reduced resistance against M. oryzae. Strikingly, AvrPiz-t interferes with the association of OsAKT1 with its upstream regulator, the cytoplasmic kinase OsCIPK23, which also plays a positive role in K+ absorption and resistance to M. oryzae. Furthermore, we show a direct correlation between blast disease resistance and external K+ status in rice plants. Together, our data present a novel mechanism by which a pathogen suppresses plant host immunity by modulating a host K+ channel.

Ca is absorbed by roots and transported upward through the xylem to the apoplastic space of the leaf, after which it is deposited into the leaf cell. In Arabidopsis (Arabidopsis thaliana), the tonoplast-localized Ca/H transporters CATION EXCHANGER1 (CAX1) and CAX3 sequester Ca from the cytosol into the vacuole, but it is not known what transporter mediates the initial Ca influx from the apoplast to the cytosol. Here, we report that Arabidopsis CYCLIC NUCLEOTIDE-GATED CHANNEL2 (CNGC2) encodes a protein with Ca influx channel activity and is expressed in the leaf areas surrounding the free endings of minor veins, which is the primary site for Ca unloading from the vasculature and influx into leaf cells. Under hydroponic growth conditions, with 0.1 mm Ca, both Arabidopsis cngc2 and cax1cax3 loss-of-function mutants grew normally. Increasing the Ca concentration to 10 mm induced HO accumulation, cell death, and leaf senescence and partially suppressed the hypersensitive response to avirulent pathogens in the mutants but not in the wild type. In vivo apoplastic Ca overaccumulation was found in the leaves of cngc2 and cax1cax3 but not the wild type under the 10 mm Ca condition, as monitored by Oregon Green BAPTA 488 5N, a low-affinity and membrane-impermeable Ca probe. Our results indicate that CNGC2 likely has no direct roles in leaf development or the hypersensitive response but, instead, that CNGC2 could mediate Ca influx into leaf cells. Finally, the in vivo extracellular Ca imaging method developed in this study provides a new tool for investigating Ca dynamics in plant cells.

Seed-setting rate is a critical determinant of grain yield in rice (Oryza sativa L.). Rapid and healthy pollen tube growth in the style is required for high seed-setting rate. The molecular mechanisms governing this process remain largely unknown. In this study, we isolate a dominant low seed-setting rate rice mutant, sss1-D. Cellular examination results show that pollen tube growth is blocked in about half of the mutant styles. Molecular cloning and functional assays reveals that SSS1-D encodes OsCNGC13, a member of the cyclic nucleotide-gated channel family. OsCNGC13 is preferentially expressed in the pistils and its expression is dramatically reduced in the heterozygous plant, suggesting a haploinsufficiency nature for the dominant mutant phenotype. We show that OsCNGC13 is permeable to Ca2+. Consistent with this, accumulation of cytoplasmic calcium concentration ([Ca2+]cyt) is defective in the sss1-D mutant style after pollination. Further, the sss1-D mutant has altered extracellular matrix (ECM) components and delayed cell death in the style transmission tract (STT). Based on these results, we propose that OsCNGC13 acts as a novel maternal sporophytic factor required for stylar [Ca2+]cyt accumulation, ECM components modification and STT cell death, thus facilitating the penetration of pollen tube in the style for successful double fertilization and seed-setting in rice.