The Xanthomonas type-III effector protein XopS stabilizes CaWRKY40a to regulate defense hormone responses and preinvasion immunity in pepper (Capsicum annuum)

A critical component of plant immunity against invading pathogens is the rapid transcriptional reprogramming of the attacked cell to minimize virulence. Many adapted plant bacterial pathogens use type III effector (T3E) proteins to interfere with plant defense responses, including the induction of i...

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Published inbioRxiv
Main Authors Raffeiner, Margot, Üstün, Suayib, Guerra, Tiziana, Spinti, Daniela, Fitzner, Maria, Sonnewald, Sophia, Baldermann, Susanne, Börnke, Frederik
Format Paper
LanguageEnglish
Published Cold Spring Harbor Cold Spring Harbor Laboratory Press 01.04.2021
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Summary:A critical component of plant immunity against invading pathogens is the rapid transcriptional reprogramming of the attacked cell to minimize virulence. Many adapted plant bacterial pathogens use type III effector (T3E) proteins to interfere with plant defense responses, including the induction of immunity genes. The elucidation of effector function is essential to understanding bacterial pathogenesis. Here, we show that XopS, a T3E of Xanthomonas campestris pv. vesicatoria (Xcv), interacts with and inhibits the proteasomal degradation of the transcriptional regulator of defense gene expression WRKY40. Virus-induced gene silencing of WRKY40 in pepper enhanced plant tolerance towards Xcv infection, indicating it represses immunity. Stabilization of WRKY40 by XopS reduces the expression of its targets including salicylic acid (SA)-responsive genes and the jasmonic acid (JA) signaling repressor JAZ8. Xcv bacteria lacking XopS display significantly reduced virulence when surface inoculated onto susceptible pepper leaves. XopS delivery by Xcv, as well as ectopic expression of XopS in Arabidopsis or Nicotiana benthamiana prevented stomatal closure in response to bacteria and biotic elicitors in a WRKY40 dependent manner. This suggests that XopS interferes with preinvasion as well as with apoplastic defense by manipulating WRKY40 stability and gene expression eventually altering phytohormone crosstalk to promote pathogen proliferation. Competing Interest Statement The authors have declared no competing interest.
DOI:10.1101/2021.03.31.437833