TY  - BOOK
AU  - Wang Z.
AU  - Li L.
AU  - Khan D.
AU  - Chen Y.
AU  - Pu X.
AU  - Wang X.
AU  - Guan M.
AU  - Rengel Z.
AU  - Chen Q.
TI  - Nitric oxide acts downstream of reactive oxygen species in phytomelatonin receptor 1 (PMTR1)-mediated stomatal closure in Arabidopsis
T2  - Journal of Plant Physiology. 282, 153917, 2023, 10.1016/j.jplph.2023.153917
KW  - ARABIDOPSIS THALIANA
KW  - MELATONIN
KW  - NITRIC OXIDE
KW  - PMTR1
KW  - ROS
KW  - STOMATAL CLOSURE
N2  - Reactive oxygen species (ROS) and nitric oxide (NO) are important signaling molecules regulating stomatal movements in plants. Melatonin (N-acetyl-5-methoxytryptamine) was found to induce stomatal closure via phytomelatonin receptor 1 (PMTR1)-mediated activation of ROS production. Here, we evaluated the interaction between ROS and NO in the melatonin-induced stomatal closure in Arabidopsis. The results showed that the exogenous melatonin-induced stomatal closure and NO production were abolished by carboxy-PTIO (cPTIO, a NO scavenger). Additionally, the mutant lines nitrate reductase 1 and 2 (nia1nia2) and NO-associated 1 (noa1) did not show melatonin-induced stomatal closure, indicating that the melatonin-mediated stomatal closure is dependent on NO. The application of H2O2 induced the NO production and stomatal closure in the presence or absence of melatonin. However, the melatonin-induced NO production was impaired in the rhohC and rbohD/F (NADPH oxidase respiratory burst oxidase homologs) mutant plants. Furthermore, the ROS levels in nia1nia2 and noa1 did not differ significantly from the wild type plants, indicating that NO is a downstream component in the melatonin-induced ROS production. Exogenous melatonin did not induce NO and ROS production in the guard cells of pmtr1 mutant lines, suggesting NO occurs downstream of ROS in the PMTR1-mediated stomatal closure in Arabidopsis. Taken together, the results presented here suggest that melatonin-induced stomatal closure via PMTR1-mediated signaling in the regulation of ROS and NO production in Arabidopsis. © 2023 Elsevier GmbH
UR  - https://drive.google.com/file/d/1Ldm6pMSdx2JkVbjxeyc04jy-2L-gwnHm/view?usp=drivesdk
ER  -