Disease Lesion Mimicry Caused by Mutations in the Rust Resistance Gene rp1

Hu, Gongshe; Richter, Todd; Hulbert, Scot H.; Pryor, Tony

doi:10.2307/3870307

Cited by 66 publications

(48 citation statements)

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“…A homolog of the Pto resistance gene (Fen) triggers a resistancelike reaction in response to herbicide application (36). Disease lesion mimic mutants, which likely arose from recombination between linked R genes, have been identified at the maize RP1 resistance gene complex (37). These examples suggest that the same mechanisms that accelerate the evolution of novel resistance genes may also generate disadvantageous alleles.…”

Section: Discussionmentioning

confidence: 99%

Independent deletions of a pathogen-resistance gene in Brassica and Arabidopsis

Grant

McDowell

Sharpe

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

120

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Plant disease resistance (R) genes confer race-specific resistance to pathogens and are genetically defined on the basis of intra-specific functional polymorphism. Little is known about the evolutionary mechanisms that generate this polymorphism. Most R loci examined to date contain alternate alleles and͞or linked homologs even in disease-susceptible plant genotypes. In contrast, the resistance to Pseudomonas syringae pathovar maculicola (RPM1) bacterial resistance gene is completely absent (rpm1-null) in 5͞5 Arabidopsis thaliana accessions that lack RPM1 function. The rpm1-null locus contains a 98-bp segment of unknown origin in place of the RPM1 gene. We undertook comparative mapping of RPM1 and f lanking genes in Brassica napus to determine the ancestral state of the RPM1 locus. We cloned two B. napus RPM1 homologs encoding hypothetical proteins with Ϸ81% amino acid identity to Arabidopsis RPM1. Collinearity of genes f lanking RPM1 is conserved between B. napus and Arabidopsis. Surprisingly, we found four additional B. napus loci in which the f lanking marker synteny is maintained but RPM1 is absent. These B. napus rpm1-null loci have no detectable nucleotide similarity to the Arabidopsis rpm1-null allele. We conclude that RPM1 evolved before the divergence of the Brassicaceae and has been deleted independently in the Brassica and Arabidopsis lineages. These results suggest that functional polymorphism at R gene loci can arise from gene deletions.

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Section: Discussionmentioning

confidence: 99%

Independent deletions of a pathogen-resistance gene in Brassica and Arabidopsis

Grant

McDowell

Sharpe

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

120

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“…Since lesion-mimic mutants form brown spots as a result of cell death, and some exhibit resistance to some pathogens, they are useful for investigating mechanisms of disease resistance. Therefore, lesion-mimic mutants have been isolated and characterized in many plant species , including Arabidopsis (Greenberg and Ausubel 1993;Dietrich et al 1994Dietrich et al , 1997Greenberg et al 1994;Weymann et al 1995;Rate et al 1999), maize (Johal et al 1995;Hu et al 1996;Gray et al 1997), barley (Jørgensen 1992;Wolter et al 1993;Büschges et al 1997), and rice (Sekiguchi and Furuta 1965;Kiyosawa 1970;Marchetti et al 1983;Takahashi et al 1999;Arase et al 2000;Yin et al 2000).…”

Section: Introductionmentioning

confidence: 99%

Differential expression of disease resistance in rice lesion-mimic mutants

et al. 2002

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Lesion-mimic mutants are useful for investigating mechanisms of disease resistance. We have characterized five lesion-mimic mutants of rice (Oryza sativa L.): spotted leaf 5-2 (spl5-2), Spl12, spl13, spl14, and Spl15, that have broad-spectrum resistance to the rice blast fungus Magnaporthe grisea and the bacterial blight pathogen Xanthomonas campestris pv. oryzae. Autofluorescence, a sign of disease resistance response, was detected in leaf-sheath cells of the spl mutants in the absence of pathogens. In addition, three pathogenesisrelated genes, PBZ1, PR1, and Cht3, were expressed in spl5-2, Spl12, and Spl15 after the appearance of lesionmimicry. In contrast, expression of these genes in spl13 and spl14 started before lesion formation. Interestingly, in spl13 and spl14, enhanced resistance to rice blast and bacterial blight was also induced before the appearance of lesion-mimicry. These results demonstrate that disease resistance is differently expressed in the spl mutants.

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“…RP1 in maize encodes an NBS-LRR (nucleotide binding site-leucine-rich repeat)-type resistance protein (10). All of these gene mutants had improved resistance to pathogens when lesions developed (5,(11)(12)(13). This fact suggests that these genes are related to the control of cell death in the pathogen-defense response in plants.…”

mentioning

confidence: 99%

A rice spotted leaf gene, Spl7 , encodes a heat stress transcription factor protein

Yamanouchi

Yano

Lin

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

301

234

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A rice spotted leaf (lesion-mimic) gene, Spl7, was identified by map-based cloning. High-resolution mapping with cleaved amplified polymorphic sequence markers enabled us to define a genomic region of 3 kb as a candidate for Spl7. We found one ORF that showed high similarity to a heat stress transcription factor (HSF). Transgenic analysis verified the function of the candidate gene for Spl7: leaf spot development was suppressed in spl7 mutants with a wild-type Spl7 transgene. Thus, we conclude that Spl7 encodes the HSF protein. The transcript of spl7 was observed in mutant plants. The levels of mRNAs (Spl7 in wild type and spl7 in mutant) increased under heat stress. Sequence analysis revealed only one base substitution in the HSF DNA-binding domain of the mutant allele, causing a change from tryptophan to cysteine.

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Disease Lesion Mimicry Caused by Mutations in the Rust Resistance Gene rp1

Cited by 66 publications

References 0 publications

Independent deletions of a pathogen-resistance gene in Brassica and Arabidopsis

Independent deletions of a pathogen-resistance gene in Brassica and Arabidopsis

Differential expression of disease resistance in rice lesion-mimic mutants

A rice spotted leaf gene, Spl7 , encodes a heat stress transcription factor protein

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