4.8 Article

The host exocyst complex is targeted by a conserved bacterial type-III effector that promotes virulence

Journal

PLANT CELL
Volume 34, Issue 9, Pages 3400-3424

Publisher

OXFORD UNIV PRESS INC
DOI: 10.1093/plcell/koac162

Keywords

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Funding

  1. Hellenic Foundation for Research and Innovation (HFRI) [4776]
  2. General Secretariat for Research and Technology (GSRT) [4776]
  3. IMBB-FORTH
  4. European Union
  5. Operational Program Competitiveness, Entrepreneurship and Innovation [T1EDK-01878]
  6. FORMAS Research Council [MOP-86675]
  7. HFRI [1624]
  8. iNEXT-Discovery - Horizon 2020 program of the European Commission [871037]

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This article investigates the mechanism by which Xanthomonas campestris evades host defense responses by targeting the plant exocyst complex through its core effector XopP. XopP inhibits exocytosis and suppresses plant immune responses, promoting successful infection.
XopP, a core bacterial effector of Xanthomonas campestris, manipulates the plant exocyst complex bypassing several host defense responses. For most Gram-negative bacteria, pathogenicity largely depends on the type-III secretion system that delivers virulence effectors into eukaryotic host cells. The subcellular targets for the majority of these effectors remain unknown. Xanthomonas campestris, the causal agent of black rot disease of crucifers such as Brassica spp., radish, and turnip, delivers XopP, a highly conserved core-effector protein produced by X. campestris, which is essential for virulence. Here, we show that XopP inhibits the function of the host-plant exocyst complex by direct targeting of Exo70B, a subunit of the exocyst complex, which plays a significant role in plant immunity. XopP interferes with exocyst-dependent exocytosis and can do this without activating a plant NOD-like receptor that guards Exo70B in Arabidopsis. In this way, Xanthomonas efficiently inhibits the host's pathogen-associated molecular pattern (PAMP)-triggered immunity by blocking exocytosis of pathogenesis-related protein-1A, callose deposition, and localization of the FLAGELLIN SENSITIVE2 (FLS2) immune receptor to the plasma membrane, thus promoting successful infection. Inhibition of exocyst function without activating the related defenses represents an effective virulence strategy, indicating the ability of pathogens to adapt to host defenses by avoiding host immunity responses.

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