Signaling for immunity

To identify defence signaling components, we make use of the Arabidopsis syntaxin double mutant, pen1 syp122, which is “lesion-mimic” as it permanently expresses immunity. pen1 syp122 plants were re-mutagenized, and from this screen we established a mutant collection of ~ 200 pen1 syp122 ssd triple mutant lines, in which the ssd mutations reduce the level of autoimmunity.

We use next generation-sequencing to identify the mutated genes, and today we know the identity of about 90 mutant alleles from 15 SSD genes. Our current focus is on SSD5 and SSD6. They both encode proteins associated with membrane lipids, and their requirement for immunity has not previously been shown. Lesion-mimic phenotypes can be activated by NLR-type intracellular receptors turned on by mutation of effector targets, and interestingly, data suggest that SSD5 and SSD6 function upstream of such an unknown NLR. We now aim to uncover the precise mechanisms of SSD5 and SSD6, and to identify the NLR that activate the lesion-mimic phenotype of pen1 syp122.

The functional relationship between powdery mildew effectors and barley NLR proteins is being studied to learn how resistance genes that encode such intracellular receptors prevent disease.

We have coincidentally found that certain wheat cultivars respond strongly to the type-3 secretion system (T3SS) of Pseudomonas syringae plant pathogenic bacteria. A genome-wide association study revealed that a single gene in wheat is responsible for this response, and we aim at identifying this gene. Meanwhile, the T3SS consists of approximately 25 bacterial proteins, and our current activities as well focus on precise identification of the recognized bacterial protein.

Wheat leaves infiltrated with Pseudomonas expressing T3SS













Project participants

Name Title Phone E-mail
Xuan Li Research Assistant +4535333810 E-mail

Contact research group leader

Hans Thordal-ChristensenHans Thordal-Christensen
Professor WSR
Ph: +45 35 33 34 43