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Methyl jasmonate inhibits lamina joint inclination by repressing brassinosteroid biosynthesis and signaling in rice

Gan, Lijun, Wu, Hong, Wu, Dapeng, Zhang, Zhanfang, Guo, Zhengfei, Yang, Na, Xia, Kai, Zhou, Xie, Oh, Keimei, Matsuoka, Makoto, Ng, Denny, Zhu, Changhua
Plant science 2015 v.241 pp. 238-245
Oryza sativa, auxins, biosynthesis, brassinosteroids, culms, ethylene, gene expression, genes, gibberellins, leaf angle, leaf blade, lithium, messenger RNA, methyl jasmonate, mutants, plant architecture, rice, signal transduction
Lamina joint inclination or leaf angle (the angle between the leaf blade and vertical culm) is a major trait of rice plant architecture. The plant hormone brassinosteroid (BR) is the main regulator of this trait, while other plant hormones, including ethylene, gibberellin, and auxin, also influence leaf angle. In this study, we found that methyl jasmonate (MeJA) also participates in regulating lamina joint inclination. MeJA decreased lamina joint inclination and inhibited the BR-induced increase in lamina joint inclination. Furthermore, addition of a BR synthesis inhibitor increased the extent of change in lamina joint inclination in response to treatment with a low concentration of MeJA (0.05 or 0.5mgL−1), but it did not alter the lamina joint inclination of plants treated with a high concentration of MeJA (5mgL−1). Further studies showed that MeJA treatment significantly repressed the expression of BR biosynthesis-related genes and decreased endogenous BRs levels. In addition, the lamina joint inclination in the OsBRI1 mutant d61-1 was less sensitive to MeJA compared with its wild type counterpart, and lithium chloride-induced inactivation of GSK3-like kinase, a negative regulator of BR signaling, partly rescued the MeJA-induced reduction in lamina joint inclination. Further studies showed that MeJA treatment reduced the mRNA levels of BR signaling and target genes. These results indicate that MeJA-inhibition of lamina joint inclination may depend on BR biosynthesis and the BR signaling pathway.