Phytophthora infestans Avirulence Gene Avr4 Encodes an RXLR-dEER Effector

Resistance in potato against the oomycete Phytophthora infestans is conditioned by resistance (R) genes that are introgressed from wild Solanum spp. into cultivated potato. According to the gene-for-gene model, proteins encoded by R genes recognize race-specific effectors resulting in a hypersensiti...

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Published in:Molecular plant-microbe interactions Vol. 21; no. 11; pp. 1460 - 1470
Main Authors: Poppel, Pieter M.J.A. van, Guo, Jun, Vondervoort, Peter J.I. van de, Jung, Maartje W.M, Birch, Paul R.J, Whisson, Stephen C, Govers, Francine
Format: Journal Article
Language:English
Published: St Paul, MN APS Press 01-11-2008
The American Phytopathological Society
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Summary:Resistance in potato against the oomycete Phytophthora infestans is conditioned by resistance (R) genes that are introgressed from wild Solanum spp. into cultivated potato. According to the gene-for-gene model, proteins encoded by R genes recognize race-specific effectors resulting in a hypersensitive response (HR). We isolated P. infestans avirulence gene PiAvr4 using a combined approach of genetic mapping, transcriptional profiling, and bacterial artificial chromosome marker landing. PiAvr4 encodes a 287-amino-acid-protein that belongs to a superfamily of effectors sharing the putative host-cell-targeting motif RXLR-dEER. Transformation of P. infestans race 4 strains with PiAvr4 resulted in transformants that were avirulent on R4 potato plants, demonstrating that PiAvr4 is responsible for eliciting R4-mediated resistance. Moreover, expression of PiAvr4 in R4 plants using PVX agroinfection and agroinfiltration showed that PiAvr4 itself is the effector that elicits HR on R4 but not r0 plants. The presence of the RXLR-dEER motif suggested intracellular recognition of PiAvr4. This was confirmed in agroinfiltration assays but not with PVX agroinfection. Because there was always recognition of PiAvr4 retaining the signal peptide, extracellular recognition cannot be excluded. Deletion of the RXLR-dEER domain neither stimulated nor prevented elicitor activity of PiAvr4. Race 4 strains have frame shift mutations in PiAvr4 that result in truncated peptides; hence, PiAvr4 is apparently not crucial for virulence.
Bibliography:http://dx.doi.org/10.1094/MPMI-21-11-1460
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ISSN:0894-0282
1943-7706
DOI:10.1094/MPMI-21-11-1460