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Published on: May 21, 2019
PEPR1 Mediates SsNLP1-Triggered Immunity Against Sclerotinia sclerotiorum
Imtiaz Ahmad Sajid1, Muhammad Kamran2, Zeeshan Ghulam Nabi Gishkori1
1Zhejiang Key Laboratory of Biology and Ecological Regulation of Crop Pathogens and Insects, Institute of Biotechnology, College of Agriculture and Biotechnology, Zhejiang University, 866 Yu Hang Tang Road, Hangzhou 310058, China.
Abstract:
Necrosis- and ethylene-inducing peptide 1 (Nep1)-like proteins (NLPs) are conserved microbial proteins that contain immunogenic patterns capable of activating plant pattern-triggered immunity (PTI). NLP patterns from Sclerotinia sclerotiorum (SsNLPs), a destructive necrotrophic fungal pathogen with a broad host range, have been identified, and their roles in PTI have been revealed. Nevertheless, the molecular mechanisms by which SsNLPs stimulate plant immunity remain largely unknown. In this study, we phylogenetically characterized SsNLPs and demonstrated the involvement of the phytocytokine receptor-like kinases PEPRs in SsNLP1-triggered immunity. SsNLPs contained the NPP1 domain and GHRHDWE motif and were phylogenetically closely associated with Botrytis cinerea NLPs. SsNLP1 treatment strongly induced the expression of PEPR genes. Further genetic analyses using Arabidopsis wild-type, pepr1 pepr2 double mutant, and PEPR1 overexpression lines showed that SsNLP1 elicited diverse immune responses, including reactive oxygen species (ROS) accumulation and defense gene activation, and induced plant resistance to S. sclerotiorum. Notably, the induced plant resistance and immune responses were strengthened in PEPR1 overexpression lines and significantly reduced in the pepr1 pepr2 mutant, indicating a positive role of PEPR signaling in SsNLP1-triggered immunity. Overall, our results revealed that phytocytokine PEPR1 signaling amplifies PAMP SsNLP1-triggered immunity, thereby enhancing resistance against S. sclerotiorum. Our findings provide an example of the coordination between PAMP- and phytocytokine-triggered immunity for robust resistance to a necrotrophic pathogen.
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