OsJAZ10 negatively modulates the drought tolerance by integrating hormone signaling with systemic electrical activity in rice.

Jasmonic acid (JA) plays crucial functions in plant stress response, and the synergistic interaction between JA and abscisic acid (ABA) signaling is implicated to help plants adapt to environmental challenges, whereas the underlying molecular mechanism still needs to be revealed. Here, we report that OsJAZ10, a repressor in the JA signaling, represses rice drought tolerance via inhibition of JA and ABA biosynthesis. Function loss of OsJAZ10 markedly enhances, while overexpression of OsJAZ10ΔJas reduces rice drought tolerance. The osjaz10 mutant is more sensitive to exogenous ABA and MeJA, and produces higher levels of ABA and JA after drought treatment, indicating OsJAZ10 represses the biosynthesis of these two hormones. Mechanistic study demonstrated that OsJAZ10 physically interacts with OsMYC2. Transient transcriptional regulation assays showed that OsMYC2 activates the expression of ABA-biosynthetic gene OsNCED2, JA-biosynthetic gene OsAOC, and drought-responsive genes OsRAB21 and OsLEA3, while OsJAZ10 prevents OsMYC2 transactivation of these genes. Further, the electrophoretic mobility shift assay (EMSA) confirmed that OsMYC2 directly binds to the promoters of OsNCED2 and OsRAB21. Electrical activity has been proposed to activate JA biosynthesis. Interestingly, OsJAZ10 inhibits the propagation of osmotic stress-elicited systemic electrical signals, indicated by the significantly increased PEG-elicited slow wave potentials (SWPs) in osjaz10 mutant, which is in accordance with the elevated JA levels. Collectively, our findings establish that OsJAZ10 functions as a negative regulator in rice drought tolerance by repressing JA and ABA biosynthesis, and reveal an important mechanism that plants integrate electrical events with hormone signaling to enhance the adaption to environmental stress.

Histone deacetylase OsHDA716 represses rice chilling tolerance by deacetylating OsbZIP46 to reduce its transactivation function and protein stability.

Low temperature is a major environmental factor limiting plant growth and crop production. Epigenetic regulation of gene expression is important for plant adaptation to environmental changes, whereas the epigenetic mechanism of cold signaling in rice (Oryza sativa) remains largely elusive. Here, we report that the histone deacetylase (HDAC) OsHDA716 represses rice cold tolerance by interacting with and deacetylating the transcription factor OsbZIP46. The loss-of-function mutants of OsHDA716 exhibit enhanced chilling tolerance, compared with the wild-type plants, while OsHDA716 overexpression plants show chilling hypersensitivity. On the contrary, OsbZIP46 confers chilling tolerance in rice through transcriptionally activating OsDREB1A and COLD1 to regulate cold-induced calcium influx and cytoplasmic calcium elevation. Mechanistic investigation showed that OsHDA716-mediated OsbZIP46 deacetylation in the DNA-binding domain reduces the DNA-binding ability and transcriptional activity as well as decreasing OsbZIP46 protein stability. Genetic evidence indicated that OsbZIP46 deacetylation mediated by OsHDA716 reduces rice chilling tolerance. Collectively, these findings reveal that the functional interplay between the chromatin regulator and transcription factor fine-tunes the cold response in plant and uncover a mechanism by which HDACs repress gene transcription through deacetylating nonhistone proteins and regulating their biochemical functions.

OsNAC120 balances plant growth and drought tolerance by integrating GA and ABA signaling in rice.

The crosstalk between gibberellin (GA) and abscisic acid (ABA) signaling is crucial for balancing plant growth and adaption to environmental stress. Nevertheless, the molecular mechanism of their mutual antagonism still remains to be fully clarified. In this study, we found that knockout of the rice NAC (NAM, ATAF1/2, CUC2) transcription factor gene OsNAC120 inhibits plant growth but enhances drought tolerance, whereas OsNAC120 overexpression produces the opposite results. Exogenous GA can rescue the semi-dwarf phenotype of osnac120 mutants, and further study showed that OsNAC120 promotes GA biosynthesis by transcriptionally activating the GA biosynthetic genes OsGA20ox1 and OsGA20ox3. The DELLA protein SLENDER RICE1 (SLR1) interacts with OsNAC120 and impedes its transactivation ability, and GA treatment can remove the inhibition of transactivation activity caused by SLR1. On the other hand, OsNAC120 negatively regulates rice drought tolerance by repressing ABA-induced stomatal closure. Mechanistic investigation revealed that OsNAC120 inhibits ABA biosynthesis via transcriptional repression of the ABA biosynthetic genes OsNCED3 and OsNCED4. Rice OSMOTIC STRESS/ABA-ACTIVATED PROTEIN KINASE 9 (OsSAPK9) physically interacts with OsNAC120 and mediates its phosphorylation, which results in OsNAC120 degradation. ABA treatment accelerates OsNAC120 degradation and reduces its transactivation activity. Together, our findings provide evidence that OsNAC120 plays critical roles in balancing GA-mediated growth and ABA-induced drought tolerance in rice. This research will help us to understand the mechanisms underlying the trade-off between plant growth and stress tolerance and to engineer stress-resistant, high-yielding crops.