Abstract
This work analyses the genetic variation and evolutionary patterns of recessive resistance loci involved in matching-allele (MA) host-pathogen interactions, focusing on the pvr2 resistance gene to potyviruses of the wild pepper Capsicum annuum glabriusculum (chiltepin). Chiltepin grows in a variety of wild habitats in Mexico, and its cultivation in home gardens started about 25 years ago. Potyvirus infection of Capsicum plants requires the physical interaction of the viral VPg with the pvr2 product, the translation initiation factor eIF4E1. Mutations impairing this interaction result in resistance, according to the MA model. The diversity of pvr2/eIF4E1 in wild and cultivated chiltepin populations from six biogeographical provinces in Mexico was analysed in 109 full-length coding sequences from 97 plants. Eleven alleles were found, and their interaction with potyvirus VPg in yeast-two-hybrid assays, plus infection assays of plants, identified six resistance alleles. Mapping resistance mutations on a pvr2/eIF4E1 model structure showed that most were around the cap-binding pocket and strongly altered its surface electrostatic potential, suggesting resistance-associated costs due to functional constraints. The pvr2/eIF4E1 phylogeny established that susceptibility was ancestral and resistance was derived. The spatial structure of pvr2/eIF4E1 diversity differed from that of neutral markers, but no evidence of selection for resistance was found in wild populations. In contrast, the resistance alleles were much more frequent, and positive selection stronger, in cultivated chiltepin populations, where diversification of pvr2/eIF4E1 was higher. This analysis of the genetic variation of a recessive resistance gene involved in MA host-pathogen interactions in populations of a wild plant show that evolutionary patterns differ according to the plant habitat, wild or cultivated. It also demonstrates that human management of the plant population has profound effects on the diversity and the evolution of the resistance gene, resulting in the selection of resistance alleles.
Highlights
Host-parasite interactions often show a high degree of genetic specificity, in that only a subset of parasite genotypes can infect and multiply in each host genotype [1,2,3,4,5,6]
Analyses of plant pathogen resistance have focused on R proteins, which recognize pathogen molecules triggering defenses according to a gene-for-gene interaction
Infection may require the interaction of plant and pathogen molecules, mutations impairing this interaction resulting in recessive resistance according to a matching-alleles model
Summary
Host-parasite interactions often show a high degree of genetic specificity, in that only a subset of parasite genotypes can infect and multiply in each host genotype [1,2,3,4,5,6]. The different proposed models stem from two general ones, the gene-for-gene (GFG) and the matching-alleles (MA) models, which were initially proposed to explain plant-parasite and invertebrate-parasite interactions, respectively [1,7], evidence indicates that they are not taxonomically restricted [5]. In the MA model, there is no hierarchy of resistance (infectivity) alleles, and a particular host genotype is better at resisting a subset of parasite genotypes, and worse at resisting the rest of parasite genotypes, and a parasite genotype is better at infecting a subset of host genotypes, and worse at infecting the rest [1] Both models differ in the mechanisms determining hostparasite interactions. Evidence of resistance costs has been reported for GFG interactions [10,11,12] but, to our knowledge, costs of resistance have not been analysed in MA interactions
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