4.3 Article

Different requirement of immunity pathway components by oomycete effectors-induced cell death

Journal

PHYTOPATHOLOGY RESEARCH
Volume 4, Issue 1, Pages -

Publisher

SPRINGERNATURE
DOI: 10.1186/s42483-022-00109-1

Keywords

Phytophthora; Effector-triggered immunity; RXLR; CRN; R gene

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Funding

  1. National Natural Science Foundation of China [31625023, 32072507]
  2. Fundamental Research Funds for the Central Universities [KYT202001, JCQY201904]

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Plant pathogenic oomycete species secrete effectors to manipulate plant immunity and induce cell death. This study identified some cell death-inducing effectors and their related genes in resistant plants.
Plant pathogenic oomycete species pose a worldwide threat to crop production and ecosystems. During infection, oomycete pathogens secrete a series of effectors to manipulate plant immunity. Many of these effectors, which are indicated as avirluence gene candidates, will use components of immunity pathway to induce cell death in plants. This response given by plants is known as effector-triggered immunity (ETI). The identification of avirulence genes from pathogenic oomycete species opens a way to investigating their virulence function and uncovering related R gene repertoires in resistant plants. In this study, we screened eight cell death-inducing effectors from oomycete species in N. benthamiana and tested the requirements of ETI signaling components to induce cell death. SGT1 was required for PsAvh163- and PcRXLR25-mediated cell death, while silencing NbHSP90 abolished PcRXLR25-, PsAvh163-, PsAvh241- and PsCRN63-triggered cell death. The cell death induced by the tested effectors does not depend on EDS1, NDR1, NRG1 and ADR1. PcRXLR25- and PsAvh163-induced cell death was found to require NRC2/3/4, indicating that these two effectors are avirulence protein candidates. Finally, we found that auto-activated NRC2/3/4 also required SGT1 and HSP90 to induce hypersensitive response.

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