AtMYB44 regulates WRKY70 expression and modulates antagonistic interaction between salicylic acid and jasmonic acid signaling. (10th December 2012)

• Record Type: Journal Article
• Authors: Shim, Jae Sung; Jung, Choonkyun; Lee, Sangjoon; Min, Kyunghun; Lee, Yin‐Won; Choi, Yeonhee; Lee, Jong Seob; Song, Jong Tae; Kim, Ju‐Kon; Choi, Yang Do
• Is Part Of: Plant journal. Volume 73:Number 3(2013:Feb.)
• Page Start: 483
• Page End: 495
• Publication Date: 2012-12-10
• Subjects: Plant molecular biology -- Periodicals; Plant cells and tissues -- Periodicals; Botany -- Periodicals; 580
• DOI: 10.1111/tpj.12051
• Languages: English
• ISSNs: 0960-7412

Abstract

<abstract abstract-type="main" id="tpj12051-abs-0001"> <title>Summary</title> <p>The role of <italic>AtMYB44</italic>, an R2R3 MYB transcription factor, in signaling mediated by jasmonic acid (JA) and salicylic acid (SA) is examined. <italic>AtMYB44</italic> is induced by JA through CORONATINE INSENSITIVE 1 (COI1). <italic>AtMYB44</italic> over‐expression down‐regulated defense responses against the necrotrophic pathogen <italic>Alternaria brassicicola</italic>, but up‐regulated <italic>WRKY70</italic> and <italic>PR</italic> genes, leading to enhanced resistance to the biotrophic pathogen <italic>Pseudomonas syringae</italic> pv. <italic>tomato </italic>DC3000. The knockout mutant <italic>atmyb44</italic> shows opposite effects. Induction of <italic>WRKY70</italic> by SA is reduced in <italic>atmyb44</italic> and <italic>npr1</italic>‐<italic>1</italic> mutants, and is totally abolished in <italic>atmyb44 npr1</italic>‐<italic>1</italic> double mutants, showing that <italic>WRKY70</italic> is regulated independently through both <italic>NPR1</italic> and <italic>AtMYB44</italic>. <italic>AtMYB44</italic> over‐expression does not change SA content, but <italic>AtMYB44</italic> over‐expression phenotypes, such as retarded growth, up‐regulated <italic>PR1</italic> and down‐regulated <italic>PDF1.2</italic> are reversed by SA depletion. The <italic>wrky70</italic> mutation suppressed <italic>AtMYB44</italic> over‐expression phenotypes, including up‐regulation of <italic>PR1</italic> expression and down‐regulation of <italic>PDF1.2</italic> expression. β‐estradiol‐induced expression of <italic>AtMYB44</italic> led to <italic>WRKY70</italic> activation and thus <italic>PR1</italic> activation. AtMYB44 binds to the <italic>WRKY70</italic> promoter region, indicating that <italic>AtMYB44</italic> acts as a transcriptional activator of <italic>WRKY70</italic> by directly binding to a conserved sequence element in the <italic>WRKY70</italic> promoter. These results demonstrate that <italic>AtMYB44</italic> modulates antagonistic interaction by activating SA‐mediated defenses and repressing JA‐mediated defenses through direct control of <italic>WRKY70</italic>.</p> </abstract>