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Wiley Open Access, Molecular Plant Pathology, 5(7), p. 437-448, 2006

DOI: 10.1111/j.1364-3703.2006.00342.x

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Recent insights into R gene evolution

Journal article published in 2006 by John M. McDowell ORCID, Stacey A. Simon
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

SUMMARY Plants are under strong evolutionary pressure to maintain surveillance against pathogens. Resistance (R) gene-dependent recognition of pathogen avirulence (Avr) determinants plays a major role in plant defence. Here we highlight recent insights into the molecular mechanisms and selective forces that drive the evolution of NB-LRR (nucleotide binding-leucine-rich repeat) resistance genes. New implications for models of R gene evolution have been raised by demonstrations that R proteins can detect cognate Avr proteins indirectly by 'guarding' virulence targets, and by evidence that R protein signalling is regulated by intramolecular interactions between different R functional domains. Comparative genomic surveys of NB-LRR diversity in different species have revealed ancient NB-LRR lineages that are unequally represented among plant taxa, consistent with a Birth and Death Model of evolution. The physical distribution of NB-LRRs in plant genomes indicates that tandem and segmental duplication are important factors in R gene proliferation. The majority of R genes reside in clusters, and the frequency of recombination between clustered genes can vary strikingly, even within a single cluster. Biotic and abiotic factors have been shown to increase the frequency of recombination in reporter transgene-based assays, suggesting that external stressors can affect genome stability. Fitness penalties have been associated with some R genes, and population studies have provided evidence for maintenance of ancient R allelic diversity by balancing selection. The available data suggest that different R genes can follow strikingly distinct evolutionary trajectories, indicating that it will be difficult to formulate universally applicable models of R gene evolution.