Tomato Pub17 Suppression for Lesion-Forming Pathogen Resistance
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Solution Overview
Problem
Current breeding strategies for tomatoes are ineffective against lesion-forming pathogens like Botrytis cinerea and Alternaria solani, as dominant R-genes do not confer resistance, and quantitative trait loci (QTLs) are difficult to use due to small effects and complex genetic backgrounds.
Innovation Solution
Modify tomato plants to reduce the expression or activity of the Pub17 protein, which is associated with increased resistance to lesion-forming pathogens by introducing a mutated Pub17 allele, leveraging the principle of impaired susceptibility (S) genes.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If dominant R-genes are used for disease resistance, then resistance to biotrophic pathogens is improved, but resistance to lesion-forming pathogens is not achieved
Solution Approach 1:
Instead of using dominant R-genes that recognize pathogen effectors (the conventional approach), the invention inverts the strategy by utilizing recessive susceptibility genes. When these S-genes are impaired or non-functional, the plant gains resistance to lesion-forming pathogens. This inversion resolves the contradiction by achieving broad-spectrum resistance against necrotrophs while maintaining the reliability of disease resistance through a fundamentally different genetic mechanism.
Solution Approach 2:
The invention changes the genetic parameter from dominant R-gene presence to recessive S-gene impairment. By mutating or knocking out susceptibility genes like PUB17, the plant transitions from a susceptible state to a resistant state against lesion-forming pathogens, thereby achieving broad-spectrum resistance without relying on pathogen-specific R-genes.
2Reliability
If quantitative trait loci (QTLs) are used for resistance, then resistance to lesion-forming pathogens is improved, but breeding complexity increases due to small individual effects and complex genetic backgrounds
Solution Approach 1:
The invention extracts the key resistance-determining factor from complex QTL networks by identifying and mutating a single susceptibility gene (PUB17). Instead of managing multiple QTLs with small individual effects, the approach isolates one critical gene whose impairment confers resistance, dramatically simplifying the breeding process while maintaining reliable disease resistance.
Solution Approach 2:
The invention changes the genetic architecture from polygenic QTL control to monogenic S-gene control. By focusing on a single susceptibility gene rather than multiple quantitative trait loci, the breeding complexity is reduced while achieving comparable or superior resistance levels against lesion-forming pathogens.
3Reliability
If Pub17 expression is reduced, then resistance to lesion-forming pathogens is improved, but potential impact on other plant functions must be considered
Solution Approach 1:
The invention converts the harmful effect of Pub17 (which promotes susceptibility to lesion-forming pathogens) into a beneficial resistance trait. By impairing Pub17 function, what was originally a vulnerability becomes a protective mechanism, allowing the plant to resist necrotrophic and hemi-biotrophic pathogens without apparent negative side effects on other functions.
Solution Approach 2:
The plant's natural defense system is enhanced by disrupting a susceptibility gene rather than adding external resistance mechanisms. The impaired Pub17 gene serves the plant's own interest by preventing pathogen exploitation, allowing the plant to activate its inherent defensive responses without relying on introduced R-genes or complex QTL combinations.
Data Source
AI summary
The present invention relates to novel tomato plants having improved resistance to lesion-forming pathogens caused by a reduced level, activity, or expression of Pub17 protein. The level, activity, or expression of a Pub17 protein can be reduced by modification of the Pub17 allele to contain an SNP identified to associate with increased resistance to lesion-forming pathogens. The present invention further relates to plant parts and seeds derived from said tomato plants, and to methods of making said tomato plants or increasing resistance to lesion-forming pathogens in a tomato plant, as well as use of the SNP as a marker and associated kits.