title: Deciphering the dual effect of lipopolysaccharides from plant pathogenic Pectobacterium.
abstract: Lipopolysaccharides (LPS) are a component of the outer cell surface of almost all Gram-negative bacteria and play an essential role for bacterial growth and survival. Lipopolysaccharides represent typical microbe-associated molecular pattern (MAMP) molecules and have been reported to induce defense-related responses, including the expression of defense genes and the suppression of the hypersensitive response in plants. However, depending on their origin and the challenged plant, LPS were shown to have complex and different roles. In this study we showed that LPS from plant pathogens Pectobacterium atrosepticum and Pectobacterium carotovorum subsp. carotovorum induce common and different responses in A. thaliana cells when compared to those induced by LPS from non-phytopathogens Escherichia coli and Pseudomonas aeruginosa. Among common responses to both types of LPS are the transcription of defense genes and their ability to limit of cell death induced by Pectobacterium carotovorum subsp carotovorum. However, the differential kinetics and amplitude in reactive oxygen species (ROS) generation seemed to regulate defense gene transcription and be determinant to induce programmed cell death in response to LPS from the plant pathogenic Pectobacterium. These data suggest that different signaling pathways could be activated by LPS in A. thaliana cells.
authors.affiliation: a Université Paris Diderot-Paris 7; Institut des Energies de Demain (UMR8236) ; Paris , France.
authors.forename: Kettani-Halabi
authors.initials: KH
authors.lastname: Mohamed
authors.forename: Tran
authors.initials: T
authors.lastname: Daniel
authors.forename: Dauphin
authors.initials: D
authors.lastname: Aurélien
authors.forename: Hayat
authors.initials: H
authors.lastname: El-Maarouf-Bouteau
authors.forename: Errakhi
authors.initials: E
authors.lastname: Rafik
authors.forename: Delphine
authors.initials: D
authors.lastname: Arbelet-Bonnin
authors.forename: Bernadette
authors.initials: B
authors.lastname: Biligui
authors.forename: Val
authors.initials: V
authors.lastname: Florence
authors.forename: Ennaji Moulay
authors.initials: EM
authors.lastname: Mustapha
authors.forename: Bouteau
authors.initials: B
authors.lastname: François
mesh_terms: D017360:Arabidopsis / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism; D016923:Cell Death / Q000235:genetics; D060467:Disease Resistance / Q000235:genetics; D018506:Gene Expression Regulation, Plant; D017343:Genes, Plant; D008070:Lipopolysaccharides / Q000494:pharmacology*; D016973:Pectobacterium carotovorum / Q000378:metabolism* / Q000472:pathogenicity; D010935:Plant Diseases / Q000382:microbiology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction; D014158:Transcription, Genetic
chemical_list: D008070:Lipopolysaccharides; D017382:Reactive Oxygen Species
keywords: AD, actinomycin D; Chx, cycloheximide; DPI, diphenylene iodonium; EB, Evans Blue; ETI, effector-triggered immunity; HR, hypersensitive response; LPS, lipopolysaccharides; MAMP, microbe associated molecular pattern; OPS, O-polysaccharide part; PAMP, pathogen- associated molecular pattern; PCD, programmed cell death; PTI, PAMP triggered immunity; Pa, Pectobacterium atrosepticum; Pcc, Pectobacterium carotovorum carotovorum; Pectobacterium spp; ROS, reactive oxygen species; Tiron, sodium 4,5-dihydroxybenzene-1,3-disulfonate; defense responses; lipopolysaccharides; programmed cell death; reactive oxygen species