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Plant disease-resistance proteins and the gene-for-gene concept

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Nucleotide-binding leucine-rich-repeat proteins are widespread

Jeff Ellis and co-workers have cloned the flax L alleles originally used by Flor to establish the gene-for-gene concept (Ref. [6]and J. Ellis, pers. commun.). L genes encode nucleotide-binding leucine-rich-repeat (NB–LRR) proteins that constitute the major R-protein class in gene-for-gene plant resistance. More than 30 NB–LRR-encoding genes, often members of closely linked multigene families, have now been isolated from several plant species; these proteins provide resistance to pathogens as

A biochemical model for nucleotide-binding leucine-rich-repeat proteins

NB–LRR proteins are predicted to be modular cytoplasmic molecules that consist of a C-terminal leucine-rich repeat (LRR) recognition domain connected, by a central nucleotide-binding adaptor, to various N-terminal effectors1, 18. Despite recent efforts, direct evidence for physical interaction between plant LRRs and Avr proteins is not yet available. However, LRR domains could create fast-adapting recognition surfaces for Avr signals[19]. In R proteins that possess extracellular LRRs, a

The role of Prf in the Pto signalling pathway

Currently, one of the most thought-provoking examples of gene-for-gene pathogen recognition is tomato resistance to bacterial speck disease (Fig. 1). Resistance involves recognition of an 18.3-kDa bacterial protein, AvrPto, by two host proteins, Pto and Prf15, 24. Pto is a Ser/Thr kinase that interacts physically with the AvrPto protein, can interact with and phosphorylate a second Ser/Thr kinase, Pti1 and can bind to several defence-related transcription factors, Pti4, Pti5 and Pti6. Within

Conclusion

In plants, the NB–LRR proteins specify gene-for-gene resistance to animal, fungal, bacterial and viral pathogens, and collectively constitute a comprehensive pathogen-detection system. This innate, genetic recognition–response apparatus resembles the animal immune system. R proteins might detect the association of plant pathogenicity targets with pathogen virulence factors that are then destined to become Avr products. Modification of host metabolism or suppression of basal resistance

Acknowledgements

We thank Jane Parker for in-depth discussions and for critical comments on the manuscript. The Sainsbury Laboratory is supported by the Gatsby Foundation.

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