期刊
NEW PHYTOLOGIST
卷 199, 期 1, 页码 228-240出版社
WILEY
DOI: 10.1111/nph.12256
关键词
Arabidopsis thaliana; Botrytis cinerea; lipid signalling; lysophospholipids; pathogeneses; phosphatidic acid; phospholipase D1; Pseudomonas syringae
资金
- National Science Foundation [IOS-0818740, MCB-0922879, EPS 0236913, MCB 0455318, 0920663, DBI 0521587]
- US Department of Agriculture
- Kansas Technology Enterprise Corporation
- K-IDeA Networks of Biomedical Research Excellence (INBRE) of National Institute of Health [P20RR16475]
- Kansas State University
- Div Of Molecular and Cellular Bioscience
- Direct For Biological Sciences [0920663, 0920681] Funding Source: National Science Foundation
Pathogen infection of higher plants often induces rapid production of phosphatidic acid (PA) and changes in lipid profiles, but the enzymatic basis and the function of the lipid change in pathogen-plant interactions are not well understood. Infection of phospholipase D 1 (PLD1)-deficient plants by Pseudomonas syringae tomato pv DC3000 (Pst DC30000) resulted in less bacterial growth than in wild-type plants, and the effect was more profound in virulent Pst DC3000 than avirulent Pst DC3000 (carrying the avirulence gene avrRpt2) infection. The expression levels of salicylic acid (SA)-inducible genes were higher, but those inducible by jasmonic acid (JA) showed lower expression in PLD1 mutants than in wild-type plants. However, PLD1-deficient plants were more susceptible than wild-type plants to the fungus Botrytis cinerea. The PLD1-deficient plants had lower levels of PA, JA and JA-related defense gene expression after B. cinerea inoculation. PLD1 plays a positive role in pathogen-induced JA production and plant resistance to the necrotrophic fungal pathogen B. cinerea, but a negative role in the SA-dependent signaling pathway and plant tolerance to infection with biotrophic Pst DC3000. PLD1 is responsible for most of the increase in PA production in response to necrotrophic B. cinerea and virulent Pst DC3000 infection, but contributes less to avirulent Pst DC3000 (avrRpt2)-induced PA production.
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