Multicellular living organisms and unmodified parts thereof and – Plant – seedling – plant seed – or plant part – per se – Higher plant – seedling – plant seed – or plant part
Patent
1996-09-19
1999-07-06
Campell, Bruce R.
Multicellular living organisms and unmodified parts thereof and
Plant, seedling, plant seed, or plant part, per se
Higher plant, seedling, plant seed, or plant part
800279, 800295, 435 6, 435 911, 4352523, 43525411, 4353201, 435419, 436 94, 536 236, 935 9, 935 64, 935 67, C12N 500, C12N 1500
Patent
active
059200006
DESCRIPTION:
BRIEF SUMMARY
The present invention relates to pathogen resistance in plants and more particularly the identification and use of pathogen resistance genes.
Plants are constantly challenged by potentially pathogenic microorganisms. Crop plants are particularly vulnerable, because they are usually grown as genetically uniform monocultures; when disease strikes, losses can be severe. However, most plants are resistant to most plant pathogens. To defend themselves, plants have evolved an array of both preexisting and inducible defences. Pathogens must specialize to circumvent the defence mechanisms of the host, especially those biotrophic pathogens that derive their nutrition from an intimate association with living plant cells. If the pathogen can cause disease, the interaction is said to be compatible, but if the plant is resistant, the interaction is said to be incompatible. Race specific resistance is strongly correlated with the hypersensitive response (HR), an induced response by which (it is hypothesized) the plant deprives the pathogen of living host cells by localized cell death at sites of attempted pathogen ingress.
It has long been known that HR-associated disease resistance is often (though not exclusively) specified by dominant genes (R genes). Flor showed that when pathogens mutate to overcome such R genes, these mutations are recessive. Flor concluded that for R genes to function, there must also be corresponding genes in the pathogen, denoted avirulence genes (Avr genes). To become virulent, pathogens must thus stop making a product that activates R gene-dependent defence mechanisms (Flor, 1971). A broadly accepted working hypothesis, often termed the elicitor/receptor model, is that R genes encode products that enable plants to detect the presence of pathogens, provided said pathogens carry the corresponding Avr gene (Gabriel and Rolfe, 1990). This recognition is then transduced into the activation of a defence response.
Some interactions exhibit different genetic properties. Helminthosporium carbonum races that express a toxin (Hc toxin) infect maize lines that lack the Hm1 resistance gene. Mutations to loss of Hc toxin expression are recessive, and correlated with loss of virulence, in contrast to gene-for-gene interactions in which mutations to virulence are recessive. A major accomplishment was reported in 1992, with the isolation by tagging of the Hm1 gene (Johal and Briggs, 1992). Plausible arguments have been made for how gene-for-gene interactions could evolve from toxin-dependent virulence. For example, plant genes whose products were the target of the toxin might mutate to confer even greater sensitivity to the toxin, leading to HR, and the conversion of a sensitivity gene to a resistance gene. However, this does not seem to be the mode of action of Hm1, whose gene product inactivates Hc toxin.
Pathogen avirulence genes are still poorly understood. Several bacterial Avr genes encode hydrophilic proteins with no homology to other classes of protein, while others carry repeating units whose number can be modified to change the range of plants on which they exhibit avirulence (Keen, 1992; Long and Staskawicz, 1993). Additional bacterial genes (hrp genes) are required for bacterial Avr genes to induce HR, and also for pathogenicity (Keen, 1992; Long and Staskawicz, 1993). It is not clear why pathogens make products that enable the plant to detect them. It is widely believed that certain easily discarded Avr genes contribute to but are not required for pathogenicity, whereas other Avr genes are less dispensable (Keen, 1992; Long and Staskawicz, 1993). The characterization of one fungal avirulence gene has also been reported; the Avr9 gene of Cladosporium fulvum, which confers avirulence on C. fulvum races that attempt to attack tomato varieties that carry the Cf-9 gene, encodes a secreted cysteine-rich peptide with a final processed size of 28 amino acids but its role in compatible interactions is not clear (De Wit, 1992).
The technology for gene isolation based primarily on genetic criteria has impro
REFERENCES:
JD Watson et al (1987) Molecular Biology of the Gene p. 313.
KE Hammond-Kosack et al (1994) Plant Cell 6:361-374.
Toubart et al, "Cloning and characterization of the gene encoding the endopolygalacturonase-inhibiting protein (PGIP) of Phaseolus vulgaris L.", The Plant Journal 2(3):367-373 (1992).
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Jones et al, "Isolation of the Tomato Cf-9 Gene for Resistance to Cladosporium fulvum by Transposon Tagging", Science 266:789-793 (1994).
Jones et al, "Two Complex Resistance Loci Revealed in Tomato by Classical and RFLP Mapping of the Cf-2, Cf-4, Cf-5, and Cf-9 Genes for Resistance to Cladosporium fulvum", Molecular Plant-Microbe Interactions 6(3):348-357 (1993).
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Hammond-Kosack Kim E.
Jones David A.
Jones Jonathan D. G.
Thomas Colwyn M.
Campell Bruce R.
Plant Bioscience Limited
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