Proceedings of the XLVI Italian Society of Agricultural Genetics - SIGA Annual Congress

Giardini Naxos, Italy - 18/21 September, 2002

ISBN 88-900622-3-1

Oral Communication Abstract - S5i

SIGNAL NETWORKS IN PLANT DISEASE RESISTANCE

LAMB C.

John Innes Centre, Norwich Research Park, Colney, Norwich, NR4 7UH, UK

Tel: +44 1603 450000; Fax: +44 1603 450016

chris.lamb@bbsrc.ac.uk

Attempted infection of plants by an avirulent pathogen elicits a battery of defenses often accompanied by the collapse of challenged host cells. This hypersensitive cell death results in a restricted lesion clearly delimited from surrounding healthy tissue, and is thought to contribute to the restriction of pathogen growth and spread. One of the earliest events in this hypersensitive response (HR) is the rapid generation of superoxide (O₂) and subsequent accumulation of hydrogen peroxide (H₂O₂) in an oxidative burst, reminiscent of that leading t to the production of such reactive oxygen intermediates (ROI) in activated macrophages during the mammalian innate immune response. Activation of the oxidative burst in the plant HR is a central component of a highly amplified and integrated signal system, which also involves salicylic acid and perturbations of cytosolic calcium, to trigger the expression of disease resistance mechanisms, and to mediate a systemic signal network in the establishment of plant immunity. The oxidative burst is necessary but not sufficient to trigger localised host cell death, and recent data indicate that nitric oxide (NO) co-operates with ROI in the activation of hypersensitive cell death. NO also functions independently of ROI in the induction of various defence genes including pathogenesis-related proteins and enzymes of phenylpropanoid metabolism involved in the production of lignin, antibiotics and the secondary signal salicylic acid. Recent data indicate that while plants and animals use a similar repertoire of signals in disease resistance, ROI and NO are deployed in strikingly different ways to trigger host cell death.

Local attack by a nectrotising pathogens also induces systemic acquired resistance (SAR) to a broad range of normally virulent pathogens. A genetic screen was carried out using avriulent Pseudomonas syringae pv. tomato (Pst) as infecting organism to obtain SAR-defective mutants throughout the SAR pathway in Arabidopsis thaliana. The T-DNA tagged dir1-1 (defective in induced resistance) mutant responds like wild-type plants to primary infections with both avirulent and virulent Pst. The DIR1 gene was cloned and encodes a putative non-specific lipid transfer protein. Initiation of SAR by inoculation with avirulent Pst was unaffected in dir1-1, but the ability to produce or perceive the phloem-mobile SAR signal was defective. Studies with phloem sap exudates from petioles suggested that the mobile SAR signal was absent in dir1-1 plants. We suggest that the DIR1 protein may either be the SAR mobile signal, or may transport the SAR signal to the phloem for export to distant tissue. This is the first report that genetically assigns a biological function to a lipid transfer protein and DIR1 is the first gene identified whose product is involved in SAR mobile signal production and or transport.