title: Quantitative resistance of potato to Pectobacterium atrosepticum and Phytophthora infestans: integrating PAMP-triggered response and pathogen growth.
abstract: While the mechanisms underlying quantitative resistance of plants to pathogens are still not fully elucidated, the Pathogen-Associated Molecular Patterns (PAMPs)-triggered response model suggests that such resistance depends on a dynamic interplay between the plant and the pathogen. In this model, the pathogens themselves or elicitors they produce would induce general defense pathways, which in turn limit pathogen growth and host colonisation. It therefore suggests that quantitative resistance is directly linked to a common set of general host defense mechanisms, but experimental evidence is still inconclusive. We tested the PAMP-triggered model using two pathogens (Pectobacterium atrosepticum and Phytophthora infestans) differing by their infectious processes and five potato cultivars spanning a range of resistance levels to each pathogen. Phenylalanine ammonia-lyase (PAL) activity, used as a defense marker, and accumulation of phenolics were measured in tuber slices challenged with lipopolysaccharides from P. atrosepticum or a concentrated culture filtrate from P. infestans. PAL activity increased following treatment with the filtrate but not with lipopolysaccharides, and varied among cultivars. It was positively related to tuber resistance to P. atrosepticum, but negatively related to tuber resistance to P. infestans. It was also positively related to the accumulation of total phenolics. Chlorogenic acid, the main phenolic accumulated, inhibited growth of both pathogens in vitro, showing that PAL induction caused active defense against each of them. Tuber slices in which PAL activity had been induced before inoculation showed increased resistance to P. atrosepticum, but not to P. infestans. Our results show that inducing a general defense mechanism does not necessarily result in quantitative resistance. As such, they invalidate the hypothesis that the PAMP-triggered model alone can explain quantitative resistance. We thus designed a more complex model integrating physiological host response and a key pathogen life history trait, pathogen growth, to explain the differences between the two pathosystems.
authors.affiliation: INRA (French National Institute for Agricultural Research), Agrocampus Ouest, Université de Rennes1, UMR (Mixed Research Unit) 1099 Biology of Organisms and Populations applied to Plant Protection, Rennes, France.
authors.forename: Alexander
authors.initials: A
authors.lastname: Kröner
authors.forename: Gaëlle
authors.initials: G
authors.lastname: Hamelin
authors.forename: Didier
authors.initials: D
authors.lastname: Andrivon
authors.forename: Florence
authors.initials: F
authors.lastname: Val
mesh_terms: D002726:Chlorogenic Acid / Q000494:pharmacology; D060467:Disease Resistance / Q000187:drug effects / Q000276:immunology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008954:Models, Biological; D044043:Pectobacterium / Q000187:drug effects / Q000254:growth & development*; D010636:Phenols / Q000378:metabolism; D010650:Phenylalanine Ammonia-Lyase / Q000378:metabolism; D055750:Phytophthora infestans / Q000187:drug effects / Q000254:growth & development*; D010935:Plant Diseases / Q000276:immunology* / Q000382:microbiology; D035281:Plant Tubers / Q000187:drug effects / Q000201:enzymology / Q000276:immunology / Q000382:microbiology; D051192:Receptors, Pattern Recognition / Q000378:metabolism*; D011198:Solanum tuberosum / Q000187:drug effects / Q000201:enzymology / Q000276:immunology* / Q000382:microbiology*
chemical_list: D008070:Lipopolysaccharides; D010636:Phenols; D051192:Receptors, Pattern Recognition; D002726:Chlorogenic Acid; D010650:Phenylalanine Ammonia-Lyase