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Quantitative Peptidomics Study Reveals That a Wound-Induced Peptide from PR-1 Regulates Immune Signaling in Tomato

Title
Quantitative Peptidomics Study Reveals That a Wound-Induced Peptide from PR-1 Regulates Immune Signaling in Tomato
Author(s)
Chen, Ying-LanLee, Chi-YingCheng, Kai-TanChang, Wei-HungHuang, Rong-NanNam, Hong GilChen, Yet-Ran
Issued Date
2014-10
Citation
Plant Cell, v.26, no.10, pp.4135 - 4148
Type
Article
Keywords
HYPERSENSITIVE RESPONSEENDOGENOUS PEPTIDESFUNCTIONAL GENOMICSHYDROGEN-PEROXIDEOXIDATIVE BURSTPLANT HORMONESJASMONIC ACIDDEFENSELEAVESARABIDOPSIS
ISSN
1040-4651
Abstract
Many important cell-to-cell communication events in multicellular organisms are mediated by peptides, but only a few peptides have been identified in plants. In an attempt to address the difficulties in identifying plant signaling peptides, we developed a novel peptidomics approach and used this approach to discover defense signaling peptides in plants. In addition to the canonical peptide systemin, several novel peptides were confidently identified in tomato (Solanum lycopersicum) and quantified to be induced by both wounding and methyl jasmonate (MeJA). A wounding or wounding plus MeJA-induced peptide derived from the pathogenesis-related protein 1 (PR-1) family was found to induce significant antipathogen and minor antiherbivore responses in tomato. This study highlights a role for PR-1 in immune signaling and suggests the potential application of plant endogenous peptides in efforts to defeat biological threats in crop production. As PR-1 is highly conserved across many organisms and the putative peptide from At-PR1 was also found to be bioactive in Arabidopsis thaliana, our results suggest that this peptide may be useful for enhancing resistance to stress in other plant species. © 2014 American Society of Plant Biologists. All rights reserved.
URI
http://hdl.handle.net/20.500.11750/1674
DOI
10.1105/tpc.114.131185
Publisher
American Society of Plant Biologists
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Department of New Biology CBRG(Complex Biology Research Group) 1. Journal Articles

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