Xanthomonas euvesicatoria type III effector XopQ interacts with tomato and pepper 14–3–3 isoforms to suppress effector‐triggered immunity. (26th December 2013)

• Record Type: Journal Article
• Authors: Teper, Doron; Salomon, Dor; Sunitha, Sukumaran; Kim, Jung‐Gun; Mudgett, Mary Beth; Sessa, Guido
• Is Part Of: Plant journal. Volume 77:Number 2(2014:Jan.)
• Page Start: 297
• Page End: 309
• Publication Date: 2013-12-26
• Subjects: Plant molecular biology -- Periodicals; Plant cells and tissues -- Periodicals; Botany -- Periodicals; 580
• DOI: 10.1111/tpj.12391
• Languages: English
• ISSNs: 0960-7412

Abstract

<abstract abstract-type="main" id="tpj12391-abs-0001"> <title>Summary</title> <p>Effector‐triggered immunity (ETI) to host‐adapted pathogens is associated with rapid cell death at the infection site. The plant‐pathogenic bacterium <italic>Xanthomonas euvesicatoria</italic> (<italic>Xcv</italic>) interferes with plant cellular processes by injecting effector proteins into host cells through the type III secretion system. Here, we show that the <italic>Xcv</italic> effector XopQ suppresses cell death induced by components of the ETI‐associated MAP kinase cascade MAPKKKα MEK2/SIPK and by several <italic>R</italic>/<italic>avr</italic> gene pairs. Inactivation of <italic>xopQ</italic> by insertional mutagenesis revealed that this effector inhibits ETI‐associated cell death induced by avirulent <italic>Xcv</italic> in resistant pepper (<italic>Capsicum annuum</italic>), and enhances bacterial growth in resistant pepper and tomato (<italic>Solanum lycopersicum</italic>). Using protein–protein interaction studies in yeast (<italic>Saccharomyces cerevisiae</italic>) and <italic>in planta</italic>, we identified the tomato 14–3–3 isoform SlTFT4 and homologs from other plant species as XopQ interactors. A mutation in the putative 14–3–3 binding site of XopQ impaired interaction of the effector with CaTFT4 in yeast and its virulence function <italic>in planta</italic>. Consistent with a role in ETI, <italic> TFT4</italic> mRNA abundance increased during the incompatible interaction of tomato and pepper with <italic>Xcv</italic>. Silencing of <italic>NbTFT4</italic> in <italic>Nicotiana benthamiana</italic> significantly reduced cell death induced by MAPKKKα. In addition, silencing of <italic>CaTFT4</italic> in pepper delayed the appearance of ETI‐associated cell death and enhanced growth of virulent and avirulent <italic>Xcv</italic>, demonstrating the requirement of TFT4 for plant immunity to <italic>Xcv</italic>. Our results suggest that the XopQ virulence function is to suppress ETI and immunity‐associated cell death by interacting with TFT4, which is an important component of ETI and a <italic>bona fide</italic> target of XopQ.</p> </abstract>