The Genetic Bases of Relationships between Microbial Parasites and their Hosts

Crute, I. R.

doi:10.1007/978-94-009-5145-7_5

Cited by 64 publications

(33 citation statements)

References 218 publications

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“…When parallel genetic studies have been made, specificity has often been shown to be conferred by a ''gene-for-gene'' interaction; for every gene for resistance in the host there is a matching gene for avirulence in the pathogen (Flor 1956). The gene-for-gene interaction has now been demonstrated or inferred in >20 diseases caused by taxonomically diverse pathogens and probably functions in many more (Flor 1971;Crute 1986). The gene-for-gene interaction is undoubtedly an oversimplification; however, it is a useful predictive genetic description of the interaction between plants and their pathogens.…”

Section: Classical Geneticsmentioning

confidence: 99%

Clusters of Resistance Genes in Plants Evolve by Divergent Selection and a Birth-and-Death Process

1998

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Classical genetic and molecular data show that genes determining disease resistance in plants are frequently clustered in the genome. Genes for resistance (R genes) to diverse pathogens cloned from several species encode proteins that have motifs in common. These motifs indicate that R genes are part of signal-transduction systems. Most of these R genes encode a leucine-rich repeat (LRR) region. Sequences encoding putative solvent-exposed residues in this region are hypervariable and have elevated ratios of nonsynonymous to synonymous substitutions; this suggests that they have evolved to detect variation in pathogen-derived ligands. Generation of new resistance specificities previously had been thought to involve frequent unequal crossing-over and gene conversions. However, comparisons between resistance haplotypes reveal that orthologs are more similar than paralogs implying a low rate of sequence homogenization from unequal crossing-over and gene conversion. We propose a new model adapted and expanded from one proposed for the evolution of vertebrate major histocompatibility complex and immunoglobulin gene families. Our model emphasizes divergent selection acting on arrays of solvent-exposed residues in the LRR resulting in evolution of individual R genes within a haplotype. Intergenic unequal crossing-over and gene conversions are important but are not the primary mechanisms generating variation.Plants, like animals, are continually challenged by a myriad of potential pathogens. There is increasing evidence that defense systems of plants are at least as complex as vertebrate defense systems. Unlike animals, however, plants do not have a circulatory system and therefore cannot rely on a specialized, proliferative immune system. Each plant cell has to be capable of defense, even though this defense is coordinated locally and systemically between cells. There are a variety of types of resistance genes and mechanisms, some induced and some constitutive (for review, see Godiard et al. 1994;Michelmore 1995;Hammond-Kosack and Jones 1997). Often, although not always, disease resistance in plants is determined by single, usually dominant, genes. The recent cloning of several such resistance genes (R genes) is providing insight into their function and evolution. The defense system of plants may be ancient and predate the evolution of the immune system; genes similar to plant R genes have been identified in mammals van der Biezen and Jones 1998).In this review we consider what is known about the genomic organization and evolution of disease resistance genes in plants. The picture that is emerging for the organization and evolution of plant R genes is similar to that of the vertebrate major histocompatibility complex (MHC), T-cell receptor (TCR), and immunoglobulin genes. Therefore, although the specific types of genes involved are different, the evolutionary forces shaping the plant and vertebrate defense systems may be similar. We propose a model for the evolution of plant R genes that is adapted and expanded from a m...

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Section: Classical Geneticsmentioning

confidence: 99%

Clusters of Resistance Genes in Plants Evolve by Divergent Selection and a Birth-and-Death Process

1998

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“…In each case there was evidence for the operation of an epistatic inhibitor gene modulating the expression of a dominant avirulence gene. As Crute (1985) has pointed out these examples may be indicative of an additional tier of genetic control superimposed on the generally recognized gene-for-gene pattern. The extension of such dual systems to bacterial phytopathogens provides further evidence for their generality.…”

Section: Discussionmentioning

confidence: 96%

Changes in cultivar-specificity toward pea can result from transfer of plasmid RP4 and other incompatibility group P1 replicons to Pseudomonas syringae pv. pisi.

Moulton

Vivian

Hunter

et al. 1993

Journal of General Microbiology

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Changes in cultivar-specificity toward pea can result from transfer of plasmid RP4 and other incompatibility group P1 replicons to Pseudomonas syringae pv. pisi. England, Frenchay Campus, Coldharbour Lane, Bristol BS16 IQY, UK 2Horticulture Research International, Wellesbourne, Warwick CV3.5 9EF, UK (Received 25 June 1993; revised 21 July 1993; accepted 23 July 1993) Transfer of RP4 and related replicons belonging to the Escherichia coli incompatibility group P (Pseudomonas aeruginosa IncP1) to races 2 and 6 of P. syringae pv. pisi was associated with the creation of two types of transconjugant, one resembling the parental race and the other showing an altered cultivar-specificity towards pea. The latter, irrespective of the parental race, exhibited a novel pattern of interaction with pea that corresponded to race 4; consequently such transconjugants were termed race 4-like. Curing of RP4 did not affect the phenotype, except in relation to the antibiotic resistances specified by RP4. The race 4-like strains were nonfluorescent when cultured on appropriate media (in contrast to the particular isolates of races 2 and 6 from which they were derived), showed an enhanced ability to inherit RP4 subsequently (at frequencies up to lo-' per recipient) and differed from their parental race in their pattern of plasmid profile. The plasmid profiles were similar for all race 4-like strains irrespective of origin. There was no evidence that RP4 had recombined with DNA in the recipient and probing failed to detect the retention of any part of RP4 in cured strains. The inheritance of the related cosmid vector, pLAFR3, had similar effects in races 2 and 6. This observation is important since this vector has been widely used to clone avirulence genes in plant pathogenic bacteria. Transfer of the IncW plasmids S-a and R388 did not cause any changes in the fluorescence or cultivar-specificity of races 2 or 6. The novel avirulence expressed by the race 4-like variants derived from races 2 and 6 provides evidence for the presence in races 2 and 6 of an inhibitorlsuppressor gene, which modulates the expression of the race 4-like avirulence gene. IntroductionPlant pathogenic bacteria often exhibit considerable specificity in their interactions with potential host plants. In pathovars of Pseudomonas syringae, this specificity appears to be based upon matching genes for recognition in the host and pathogen. The response of the host to invasion by the pathogen is determined by avirulence (am) genes in the pathogen and matched resistance (R) genes in the host. When a race of the pathogen carries an avr gene that is matched by the presence of an R gene in the host the interaction which occurs results in the induction of the host defence mechanism, often seen as a hypersensitive reaction. In the absence of the matching avr and R genes disease is the outcome (Keen, 1990 The cloning of avirulence genes in P. syringae pv. pisi and other pathovars (Vivian, 1992) has been based on the use of gene libraries constructed in vectors, such as...

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“…Race-specific resistance to microbial parasites in crop plants is generally under simple genie control [see Hooker & Saxena (1971), Day (1974) and Crute (1985) for general reviews]. Resistance to each race is usually conditioned by a single gene, as would be expected for a gene-for-gene system.…”

Section: Discussionmentioning

confidence: 99%

THE GENETICS OF RACE‐SPECIFIC RESISTANCE IN GROUNDSEL (SENECIO VULGARIS L.) TO THE POWDERY MILDEW FUNGUS, ERYSIPHE FISCHERI BLUMER

Harry

Clarke

1987

New Phytologist

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SUMMARYThe inheritance of race specific resistance to five pathotypes of the powdery mildew fungus Erysiphe fischeri Blumer was studied in different lines of Senecio vulgaris L. With two exceptions, resistance was dominant over susceptibility. The exceptions were two crosses in which resistance to pathotype 3 behaved as the recessive character. The data from these crosses suggested the involvement of dominant inhibitor genes which suppressed the activity of the resistance gene. Seven different dominant resistance genes were identified in three resistant lines, two conditioned resistance to pathotype 4, two to pathotype 10 and one each to pathotypes 3, 5 and 11. The two genes conditioning resistance to pathotype 4 were unlinked, as were the two conditioning resistance to pathotype 10. The genes for resistance to pathotypes 3, 5 and 11 were clearly linked in one line and were probably linked in the other two lines. The linkage group also appears to contain one of each of the genes for resistance to pathotype 4 and 10. The expression of the two genes conditioning resistance to 4 and 10, not in the main linkage group, appeared to be reduced in one line, probably due to the activity of modifier genes. The results are consistent with the hypothesis that race-specific resistance in S. vulgaris is controlled by a gene-for-gene interaction.

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The Genetic Bases of Relationships between Microbial Parasites and their Hosts

Cited by 64 publications

References 218 publications

Clusters of Resistance Genes in Plants Evolve by Divergent Selection and a Birth-and-Death Process

Clusters of Resistance Genes in Plants Evolve by Divergent Selection and a Birth-and-Death Process

Changes in cultivar-specificity toward pea can result from transfer of plasmid RP4 and other incompatibility group P1 replicons to Pseudomonas syringae pv. pisi.

THE GENETICS OF RACE‐SPECIFIC RESISTANCE IN GROUNDSEL (SENECIO VULGARIS L.) TO THE POWDERY MILDEW FUNGUS, ERYSIPHE FISCHERI BLUMER

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