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ATG4 Mediated <i>Psm</i> ES4326<i>/AvrRpt2</i>-Induced Autophagy Dependent on Salicylic Acid in <i>Arabidopsis Thaliana</i>
oleh: Wenjun Gong, Bingcong Li, Baihong Zhang, Wenli Chen
Format: | Article |
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Diterbitkan: | MDPI AG 2020-07-01 |
Deskripsi
<i>Psm</i> ES4326/<i>AvrRpt2</i> (<i>AvrRpt2</i>) was widely used as the reaction system of hypersensitive response (HR) in <i>Arabidopsis</i>. The study showed that in <i>npr1 (GFP-ATG8a)</i>, <i>AvrRpt2</i> was more effective at inducing the production of autophagosome and autophagy flux than that in <i>GFP-ATG8a</i>. The mRNA expression of <i>ATG1</i>, <i>ATG6</i> and <i>ATG8a</i> were more in <i>npr1</i> 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 <i>atg4a4b</i> (ATG4 deletion mutant) during <i>AvrRpt2</i> infection. Compared with WT, <i>atg4a4b</i> had higher expression of <i>salicylic acid glucosyltransferase 1 (SGT1)</i> and <i>isochorismate synthase 1 (ICS1)</i>; but less salicylic acid (SA) in normal condition and the same level of free SA during <i>AvrRpt2</i> infection. These results suggested that the consumption of free SA should be occurred in <i>atg4a4b</i>. <i>AvrRpt2</i> 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 <i>NPR3</i> in <i>atg4a4b</i> may accelerate the degradation of NPR1 during <i>AvrRpt2</i> infection.