No abstract

Phytomelatonin is a universal signal molecule that regulates plant growth and stress response. However, only one receptor, AtPMTR1/CAND2 that could directly bind with and perceive melatonin signaling has been identified in dicotyledon plant Arabidopsis so far, whether other plants contain phytomelatonin receptor and how it functions are still unknown. Herein, we identified a new phytomelatonin receptor from monocot maize, and investigated its role in plant osmotic and drought stress response. Using homology searching, maize plasma membrane-localized Zm00001d034063/ZmPMTR1 protein with strong binding activity to melatonin was identified as a potential phytomelatonin receptor in maize. Overexpressing ZmPMTR1 promoted osmotic stress tolerance of the wild-type Arabidopsis plant, and rescued osmotic stress sensitivity of the Arabidopsis cand2-1 mutant. Moreover, ZmPMTR1 largely rescued defect of melatonin-induced stomatal closure in the cand2-1 mutant, thereby reducing water loss rate and increasing drought stress tolerance. Furthermore, we identified a maize mutant of ZmPMTR1, EMS4-06e2fl with a point mutation causing premature termination of protein translation, and found that this maize mutant had lower leaf temperature, increased water loss rate and enhanced drought stress sensitivity. Collectively, our study reveals that ZmPMTR1, as the first identified and analyzed phytomelatonin receptor in monocot plant, functions necessarily in maize plant drought stress tolerance.

No abstract

High salinity causes ionic, osmotic, and oxidative stresses to plants, and the antioxidant enzyme Catalase2 (CAT2) plays a vital role in this process, while how CAT2 expression is regulated during plant response to high salinity remains elusive. Here, we report that phytohormone jasmonic acid (JA) impairs plant salt stress tolerance by repressing CAT2 expression in an MYC2-dependent manner. Exogenous JA application decreased plant salt stress tolerance while the jar1 mutant with reduced bioactive JA-Ile accumulation showed enhanced salt stress tolerance. JA enhanced salt-induced hydrogen peroxide (H2O2) accumulation, while treatment with H2O2-scavenger glutathione compromised such effects of JA on plant H2O2 accumulation and salt stress tolerance. In addition, JA repressed CAT2 expression in salt-stressed wild-type plant but not in myc2, a mutant of the master transcriptional factor MYC2 in JA signaling, therefore, the myc2 mutant exhibited increased salt stress tolerance. Further study showed that mutation of CAT2 largely reverted lower reactive oxygen species (ROS) accumulation, higher CAT activity, and enhanced salt stress tolerance of the myc2 mutant in myc2 cat2-1 double mutant, revealing that CAT2 functions downstream JA-MYC2 module in plant response to high salinity. Together, our study reveals that JA impairs Arabidopsis seedling salt stress tolerance through MYC2-mediated repression of CAT2 expression.

SALT OVERLY SENSITIVE1 (SOS1) is a key component of plant salt tolerance. However, how SOS1 transcription is dynamically regulated in plant response to different salinity conditions remains elusive. Here, we report that C-type Cyclin1; 1 (CycC1; 1) negatively regulates salt tolerance by interfering with WRKY75-mediated transcriptional activation of SOS1 in Arabidopsis (Arabidopsis thaliana). Disruption of CycC1; 1 promotes SOS1 expression and salt tolerance in Arabidopsis because CycC1; 1 interferes with RNA polymerase II recruitment by occupying the SOS1 promoter. Enhanced salt tolerance of the cycc1; 1 mutant was completely compromised by an SOS1 mutation. Moreover, CycC1; 1 physically interacts with the transcription factor WRKY75, which can bind to the SOS1 promoter and activate SOS1 expression. In contrast to the cycc1; 1 mutant, the wrky75 mutant has attenuated SOS1 expression and salt tolerance, whereas overexpression of SOS1 rescues the salt sensitivity of wrky75. Intriguingly, CycC1; 1 inhibits WRKY75-mediated transcriptional activation of SOS1 via their interaction. Thus, increased SOS1 expression and salt tolerance in cycc1; 1 was abolished by WRKY75 mutation. Our findings demonstrate that CycC1; 1 forms a complex with WRKY75 to inactivate SOS1 transcription under low salinity conditions. By contrast, under high salinity conditions, SOS1 transcription and plant salt tolerance is activated at least partially by increased WRKY75 expression but decreased CycC1; 1 expression.