Please use this identifier to cite or link to this item: http://223.31.159.10:8080/jspui/handle/123456789/1076
Title: Interaction of the Xanthomonas effectors XopQ and XopX results in induction of rice immune responses
Authors: Deb, Sohini
Ghosh, Palash
Patel, Hitendra K.
Sonti, Ramesh V.
Keywords: Xanthomonas oryzae pv. oryzae
14-3-3 protein
XopX
XopQ
resistance
rice
effector
Issue Date: 2020
Publisher: John Wiley & Sons
Citation: Plant Journal, 104: 332-350
Abstract: Xanthomonas oryzae pv. oryzae uses several type III secretion system (T3SS) secreted effectors, namely XopN, XopQ, XopX, and XopZ, to suppress rice immune responses that are induced following treatment with cell wall degrading enzymes. Here we show that a T3SS secreted effector XopX interacts with two of the eight rice 14‐3‐3 proteins. Mutants of XopX that are defective in 14‐3‐3 binding are also defective in suppression of immune responses, suggesting that interaction with 14‐3‐3 proteins is required for suppression of host innate immunity. However, Agrobacterium mediated delivery of both XopQ and XopX into rice cells results in induction of rice immune responses. These immune responses are not observed when either protein is individually delivered into rice cells. XopQ‐ XopX induced rice immune responses are not observed with a XopX mutant that is defective in 14‐3‐3 binding. Yeast two‐ hybrid, BiFC and co‐ IP assays indicate that XopQ and XopX interact with each other. A screen for Xanthomonas effectors which can suppress XopQ‐ XopX induced rice immune responses, led to the identification of five effectors, namely XopU, XopV, XopP, XopG and AvrBs2, that could individually suppress these immune responses. These results suggest a complex interplay of Xanthomonas T3SS effectors in suppression of both pathogen triggered immunity and effector triggered immunity to promote virulence on rice.
Description: Accepted date: 12 July 2020
URI: https://onlinelibrary.wiley.com/doi/abs/10.1111/tpj.14924
http://223.31.159.10:8080/jspui/handle/123456789/1076
ISSN: 1365-313X
Appears in Collections:Institutional Publications

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