Please use this identifier to cite or link to this item:
Type: Artigo de periódico
Title: Expression of an Oxalate Decarboxylase Impairs the Necrotic Effect Induced by Nep1-like Protein (NLP) of Moniliophthora perniciosa in Transgenic Tobacco
Author: da Silva, LF
Dias, CV
Cidade, LC
Mendes, JS
Pirovani, CP
Alvim, FC
Pereira, GAG
Aragao, FJL
Cascardo, JCM
Costa, MGC
Abstract: Oxalic acid (OA) and Nep1-like proteins (NLP) are recognized as elicitors of programmed cell death (PCD) in plants, which is crucial for the pathogenic success of necrotrophic plant pathogens and involves reactive oxygen species (ROS). To determine the importance of oxalate as a source of ROS for OA- and NLP-induced cell death, a full-length cDNA coding for an oxalate decarboxylase (FvOXDC) from the basidiomycete Flammulina velutipes, which converts OA into CO(2) and formate, was overexpressed in tobacco plants. The transgenic plants contained less OA and more formic acid compared with the control plants and showed enhanced resistance to cell death induced by exogenous OA and MpNEP2, an NLP of the hemibiotrophic fungus Moniliophthora perniciosa. This resistance was correlated with the inhibition of ROS formation in the transgenic plants inoculated with OA, MpNEP2, or a combination of both PCD elicitors. Taken together, these results have established a pivotal function for oxalate as a source of ROS required for the PCD-inducing activity of OA and NLP. The results also indicate that FvOXDC represents a potentially novel source of resistance against OA- and NLP-producing pathogens such as M. perniciosa, the causal agent of witches' broom disease of cacao (Theobroma cacao L.).
Country: EUA
Editor: Amer Phytopathological Soc
Citation: Molecular Plant-microbe Interactions. Amer Phytopathological Soc, v. 24, n. 7, n. 839, n. 848, 2011.
Rights: fechado
Identifier DOI: 10.1094/MPMI-12-10-0286
Date Issue: 2011
Appears in Collections:Unicamp - Artigos e Outros Documentos

Files in This Item:
File Description SizeFormat 
WOS000291763100009.pdf1.01 MBAdobe PDFView/Open

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.