| Literature DB >> 30466590 |
Paulina Arraño-Salinas1, José Domínguez-Figueroa2, Ariel Herrera-Vásquez3, Diego Zavala1, Joaquin Medina2, Jesús Vicente-Carbajosa2, Claudio Meneses4, Paulo Canessa3, Adrián A Moreno5, Francisca Blanco-Herrera6.
Abstract
Plants must defend themselves against pathogens. The defense response requires greater protein synthesis, which generates endoplasmic reticulum (ER) stress, yet failure to attenuate this stress has detrimental effects. WRKY7/11/17 transcription factors (TFs) are negative regulators of immunity since mutants are more resistant to Pseudomonas syringae pv tomato (Pst) infection. Here, we reveal a connection between ER-stress and the molecular mechanisms underlying the wrky mutant phenotype. The bZIP28 TF upregulates ER-chaperone expression (BiP1/2, ERdj3B, and SDF2) upon exposure of Arabidopsis to a bacterial defense elicitor, flagellin 22 (Flg22). Also, the activation of ER-chaperones is more sustained in double and triple wrky mutants treated with Flg22, suggesting that WRKY7/11/17 TFs downregulate these genes. Moreover, wrky mutants accumulate more bZIP28 transcripts in response to Flg22, indicating that WRKY7/11/17 transcriptionally repress this TF. Using Arabidopsis protoplasts, we also demonstrate that WRKYs bind to the bZIP28 promoter via W-box elements. Additionally, triple wrky mutants are more resistant, whilst bzip28 mutants are more susceptible, to Pst infection. Finally, we postulate a model of PAMP-Triggered Immunity regulation, where Flg22 activates bZIP28-signaling inducing the expression of ER-stress genes, as well as WRKY7/11/17 expression, which in turn inhibits PTI by downregulating bZIP28, controlling physiological responses in the Arabidopsis-Pst interaction.Entities:
Keywords: Basal defense response; Flg22; Unfolded protein response; WRKY; bZIP
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Year: 2018 PMID: 30466590 DOI: 10.1016/j.plantsci.2018.09.019
Source DB: PubMed Journal: Plant Sci ISSN: 0168-9452 Impact factor: 4.729