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Recent investigations in Arabidopsis thaliana suggest that SUPPRESSOR of MORE AXILLARY GROWTH 2 1 (SMAX1) and SMAX1-LIKE2 (SMXL2) are negative regulators of karrikin (KAR) and strigolactone (SL) signaling during plant growth and development, but their functions in drought resistance and related mechanisms of action remain unclear. To understand the roles and mechanisms of SMAX1 and SMXL2 in drought resistance, we investigated the drought-resistance phenotypes and transcriptome profiles of smax1 smxl2 (s1,2) double-mutant plants in response to drought stress. The s1,2 mutant plants showed enhanced drought-resistance and lower leaf water loss when compared with wild-type (WT) plants. Transcriptome comparison of rosette leaves from the s1,2 mutant and the WT under normal and dehydration conditions suggested that the mechanism related to cuticle formation was involved in drought resistance. This possibility was supported by enhanced cuticle formation in the rosette leaves of the s1,2 mutant. We also found that the s1,2 mutant plants were more sensitive to abscisic acid in assays of stomatal closure, cotyledon opening, chlorophyll degradation and growth inhibition, and they showed a higher reactive oxygen species detoxification capacity than WT plants. In addition, the s1,2 mutant plants had longer root hairs and a higher root-to-shoot ratio than the WT plants, suggesting that the mutant had a greater capacity for water absorption than the WT. Taken together, our results indicate that SMAX1 and SMXL2 negatively regulate drought resistance, and disruption of these KAR- and SL-signaling-related genes may therefore provide a novel means for improving crop drought resistance. [ABSTRACT FROM AUTHOR]

Sinapate esters, which are induced in plants under ultraviolet-B (UV-B) irradiation, have important roles not only in the protection against UV-B irradiation but also in the regulation of stomatal closure. Here, we speculated that sinapate esters would function in the stomatal closure of Arabidopsis thaliana in response to UV-B. We measured the stomatal aperture size of the wild-type (WT) and bright trichomes 1 (brt1) and sinapoylglucose accumulator 1 (sng1) mutants under UV-B irradiation; the latter two mutants are deficient in the conversion of sinapic acid to sinapoylglucose (SG) and SG to sinapoylmalate (SM), respectively. Both the brt1 and sng1 plants showed smaller stomatal apertures than the WT under normal light and UV-B irradiation conditions. The accumulation of SM and malate were induced by UV-B irradiation in WT and brt1 plants but not in sng1 plants. Consistently, exogenous malate application reduced UV-B-induced stomatal closure in WT, brt1 and sng1 plants. Nonetheless, levels of reactive oxygen species (ROS), nitric oxide (NO) and cytosolic Ca2+ were higher in guard cells of the sng1 mutant than in those of the WT under normal white light and UV-B irradiation, suggesting that disturbance of sinapate metabolism induced the accumulation of these signaling molecules that promote stomatal closure. Unexpectedly, exogenous sinapic acid application prevented stomatal closure of WT, brt1 and sng1 plants. In summary, we hypothesize that SG or other sinapate esters may promote the UV-B-induced malate accumulation and stomatal closure, whereas sinapic acid inhibits the ROS-NO pathway that regulates UV-B-induced cytosolic Ca2+ accumulation and stomatal closure. [ABSTRACT FROM AUTHOR]

Ammonium (NH4  +) is both a necessary nutrient and an important signal in plants, but can be toxic in excess. Ammonium sensing and regulatory mechanisms in plant cells have not been fully elucidated. To decipher the complex network of NH4  + signaling, we analyzed [Ca2+]cyt-associated protein kinase (CAP) genes, which encode signaling components that undergo marked changes in transcription levels in response to various stressors. We demonstrated that CAP1, a tonoplast-localized receptor-like kinase, regulates root hair tip growth by maintaining cytoplasmic Ca2+ gradients. A CAP1 knockout mutant (cap1-1) produced elevated levels of cytoplasmic NH4  +. Furthermore, root hair growth of cap1-1 was inhibited on Murashige and Skoog medium, but NH4  + depletion reestablished the Ca2+ gradient necessary for normal growth. The lower net NH4  + influx across the vacuolar membrane and relatively alkaline cytosolic pH of cap1-1 root hairs implied that mutation of CAP1 increased NH4  + accumulation in the cytoplasm. Furthermore, CAP1 functionally complemented the npr1 (nitrogen permease reactivator protein) kinase yeast mutant, which is defective in high-affinity NH4  + uptake via MEP2 (methylammonium permease 2), distinguishing CAP1 as a cytosolic modulator of NH4  + levels that participates in NH4  + homeostasis-regulated root hair growth by modulating tip-focused cytoplasmic Ca2+ gradients. [ABSTRACT FROM AUTHOR]