Analysis Of The Molecular Mechanism Of Crosstalk Between Salicylic Acid And Jasmonic Acid In Arabidopsis Thaliana

In the process of life evolution,plants have evolved an efficient immune system to protect themselves from pathogens.Plant hormones salicylic acid(SA)and jasmonic acid(JA)play important regulatory roles in plant immune system.Studies have shown that SA deficiency reduces plant resistance to biotrophic pathogens,while JA plays a role in plant resistance to necrotrophic pathogens and herbivorous insects.SA and JA constitute the backbone of hormone regulation in plant immune system.There are two parallel signal pathways of SA.On the one hand,the accumulation of SA induced by pathogens promotes the transcriptional activation of SA receptor protein NPR1,and the binding of NPR1 and TGA induced the expression of defenserelated genes.On the other hand,NPR3 and NPR4 are affected by the level of SA.When the level of SA is low,NPR3 and NPR4 act as inhibitors to inhibit the expression of defense genes.When the level of SA increases,the activities of NPR3 and NPR4 are inhibited by SA,and TGA induces the expression of downstream defense-related genes.The active form of JA in plants is JA-Ile.When plant senses external JA stimulation,JA-Ile accumulates,which promotes the ubiquitination of JAZ proteins through 26S proteasometo remove their inhibition on transcription factors,like MYC2,to activate the expression of downstream genes.However,the signal pathways of SA and JA are not independent,and there are complex interactions such as synergism and antagonism between them.The communication between different hormone signal pathways is called hormone crosstalk.Previous studies mainly focused on the antagonism of SA and JA signaling,but we found that both SA and JA can induce plant resistance to both necrotrophic bacteria Botrytis cinerea and semi-biotrophic bacteria Pseudomonas syringe pv.tomato DC3000(Pst DC3000).Whereas whether there is a crosstalk between these two induced resistances is not clear,and needs to be studied urgently.In order to explore the coordination of SA and JA signal pathways in immune induction,we analyzed the transcriptome data treated with SA or JA at different time points.SA and JA up-regulated the genes at different time points.The transcriptome data treated with SA and JA for 1 hour were analyzed in detail,and the up-regulated and downregulated gene groups were enriched respectively at this time point,and it was found that the up-regulated genes were significantly enriched to JA-related pathways after SA treatment.Then the genes induced by both SA and JA(SA-and JA-induced genes,SJIs)were analyzed.The promoter regions of these SJIs enrich the binding regions of TGA,the key transcription factor of S A signaling pathway,and MYC2,the key transcription factor of JA signaling pathway.Through mutant analysis,it was found that MYC2 and TGA played an important role in plants resistance induced by SA and JA to Pst DC3000.Previous studies have shown that NPR1 mediates plant resistance to Pst DC3000 induced by SA and JA.However,different mutantation forms of NPR1 have different sensitivity to JA,so we constructed npr1 mutants through CRISPR/Cas9 system and determined that NPR1 plays a role in JA induced immunity.Through yeast two-hybrid and the luciferase complementary assays,we didn’t detect the interaction between NPR1 and MYC2.In previous studies,tga256 has been shown to be insensitive to JA,combined with the experimental results of this project,it is suggested that SA and JA may promote the expression of SJIs through MYC2/TGA complex or MYC2/NPR1/TGA ternary complex and induce broadspectrum disease resistance in plants.In the next step,we will further confirm the role of TGA2/5/6 in JA-induced immunity,identify and analyze the role of the complex in immunity induced by SA and JA by means of molecular biology,biochemistry and genetics,to provide a new theoretical basis for analyzing the interaction between SA and JA.