ES4326/ () was widely used as the reaction system of hypersensitive response (HR) in . The study showed that in , was more effective at inducing the production of autophagosome and autophagy flux than that in . The mRNA expression of , and were more in during the early HR. Based on transcriptome data analysis, enhanced disease susceptibility 1 (EDS1) was up-regulated in wild-type (WT) but was not induced in (ATG4 deletion mutant) during infection. Compared with WT, had higher expression of and ; but less salicylic acid (SA) in normal condition and the same level of free SA during infection. These results suggested that the consumption of free SA should be occurred in . may trigger the activation of Toll/Interleukin-1 receptor (TIR)-nucleotide binding site (NB)-leucine rich repeat (LRR)-TIR-NB-LRR-to induce autophagy via EDS1, which was inhibited by nonexpressor of PR genes 1 (NPR1). Moreover, high expression of in may accelerate the degradation of NPR1 during infection.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7404177 | PMC |
http://dx.doi.org/10.3390/ijms21145147 | DOI Listing |
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