MYC2-MED25 regulates the termination of jasmine acid signals.

As an important plant hormone, jasmine acid regulates the plant's defensive response and adaptive growth.
when plants are subjected to insect attack or other adversity stress, active jasmine acid is identified by receptor COI1 (CORONATINE-INSENSITIVE 1) and releases the activity of the core transcription factor MYC2, MYC2 and transcription medium sub-MED25 form a functional complex and activates the expression of jasmine acid response gene in the whole genome, resulting in a defensive response.
but the overactivation of jasmine acid signals can consume a lot of energy and inhibit plant growth and development.
so the timely termination of jasmine acid signals is as important to plants as they are to activate.
However, at present, people's understanding of jasmine acid signaling pathway seisicity mainly focuses on signal activation, and the mechanism of termination of jasmine acid signal is still shallow.
a study by Li Chuanyou of the Institute of Genetics and Developmental Biology of the Chinese Academy of Sciences on tomato-based model, the MYC2-MED25 functional complex activates the jasmine acid signal while also regulating the termination of the jasmine acid signal.
they found that MYC2 directly activates a class of expressions of jasmine-induced bHLH transcription factorS MTB1 (MYC2-TARGETED BHLH 1), MTB2 and MTB3.
MTB1-3, on the one hand, competes with MYC2 to bind the promoter of the target gene, weakens the DNA binding ability of MYC2, and at the same time, MTB1-3 and MED25 compete competitively with MYC2, interfering with the formation of the MYC2-MED25 functional complex, thus inhibiting the transcription activation of MYC2.
so, MYC2 and MTB1-3 form a beautiful negative feedback regulatory loop that achieves the termination of jasmine acid signals.
because the expression of jasmine-induced MTB1-3 is directly controlled by MYC2 and later than MYC2 in time, the termination of jasmine acid signal is a program that is precisely "preset" by the MYC2-MED25 functional complex at the beginning of activation.
used CRISPR/Cas9 gene editing technology to obtain a tomato strain with missing MTB1-3 function.
studies have shown that the resistance of these tomato strains is significantly improved without affecting growth and development, suggesting that this finding has potential applications in insect-resistant molecular design and breeding.
the findings were published online January 4, 2019 in The Plant Cell (DOI: 10.1105/tpc.18.00405).
Plant Cell published the same period entitled Master MYCs: MYC2, the jasmonate signaling 'master switch' "In Brief", in which it reviews the important theoretical significance and application value of the results. Liu Yuanyuan, Ph.D. and Deng Lei, Ph.D. students in the
Li Chuanyou Research Group, are co-authors of the paper. Li Chuanyou, a
researcher, Yan Qingzhe, an associate researcher, and Wang Qiaomei, a professor at Zhejiang University, are co-authors.
the research was supported by the Ministry of Science and Technology, the Ministry of Agriculture and the National Natural Science Foundation of China.
Source: Institute of Genetics and Developmental Biology.