title: Botrytis cinerea manipulates the antagonistic effects between immune pathways to promote disease development in tomato.
abstract: Plants have evolved sophisticated mechanisms to sense and respond to pathogen attacks. Resistance against necrotrophic pathogens generally requires the activation of the jasmonic acid (JA) signaling pathway, whereas the salicylic acid (SA) signaling pathway is mainly activated against biotrophic pathogens. SA can antagonize JA signaling and vice versa. Here, we report that the necrotrophic pathogen Botrytis cinerea exploits this antagonism as a strategy to cause disease development. We show that B. cinerea produces an exopolysaccharide, which acts as an elicitor of the SA pathway. In turn, the SA pathway antagonizes the JA signaling pathway, thereby allowing the fungus to develop its disease in tomato (Solanum lycopersicum). SA-promoted disease development occurs through Nonexpressed Pathogen Related1. We also show that the JA signaling pathway required for tomato resistance against B. cinerea is mediated by the systemin elicitor. These data highlight a new strategy used by B. cinerea to overcome the plant's defense system and to spread within the host.
authors.affiliation: Centre de Recherche en Amélioration Végétale, Département de Biologie, Faculté des Sciences, Université de Sherbrooke, Sherbrooke, Quebec J1K 2R1, Canada.
authors.forename: Mohamed
authors.initials: M
authors.lastname: El Oirdi
authors.forename: Taha Abd
authors.initials: TA
authors.lastname: El Rahman
authors.forename: Luciano
authors.initials: L
authors.lastname: Rigano
authors.forename: Abdelbasset
authors.initials: A
authors.lastname: El Hadrami
authors.forename: María Cecilia
authors.initials: MC
authors.lastname: Rodriguez
authors.forename: Fouad
authors.initials: F
authors.lastname: Daayf
authors.forename: Adrian
authors.initials: A
authors.lastname: Vojnov
authors.forename: Kamal
authors.initials: K
authors.lastname: Bouarab
mesh_terms: D000890:Anti-Infective Agents; D020171:Botrytis / Q000378:metabolism / Q000472:pathogenicity*; D002236:Carbohydrate Conformation; D003517:Cyclopentanes / Q000378:metabolism; D023082:Defensins / Q000235:genetics / Q000378:metabolism; D005936:Glucans / Q000737:chemistry / Q000378:metabolism; D007113:Immunity, Innate / Q000276:immunology*; D018551:Solanum lycopersicum / Q000235:genetics / Q000276:immunology* / Q000382:microbiology*; D008969:Molecular Sequence Data; D054883:Oxylipins / Q000378:metabolism; D010935:Plant Diseases / Q000276:immunology* / Q000382:microbiology*; D018515:Plant Leaves / Q000276:immunology / Q000382:microbiology; D010940:Plant Proteins / Q000235:genetics / Q000378:metabolism; D030821:Plants, Genetically Modified; D020156:Salicylic Acid / Q000378:metabolism; D015398:Signal Transduction / Q000276:immunology*
chemical_list: D000890:Anti-Infective Agents; D003517:Cyclopentanes; D023082:Defensins; D005936:Glucans; D054883:Oxylipins; D010940:Plant Proteins; C011006:jasmonic acid; D020156:Salicylic Acid