title: Repression of the auxin response pathway increases Arabidopsis susceptibility to necrotrophic fungi.
abstract: In plants, resistance to necrotrophic pathogens depends on the interplay between different hormone systems, such as those regulated by salicylic acid (SA), jasmonic acid (JA), ethylene, and abscisic acid. Repression of auxin signaling by the SA pathway was recently shown to contribute to antibacterial resistance. Here, we demonstrate that Arabidopsis auxin signaling mutants axr1, axr2, and axr6 that have defects in the auxin-stimulated SCF (Skp1-Cullin-F-box) ubiquitination pathway exhibit increased susceptibility to the necrotrophic fungi Plectosphaerella cucumerina and Botrytis cinerea. Also, stabilization of the auxin transcriptional repressor AXR3 that is normally targeted for removal by the SCF-ubiquitin/proteasome machinery occurs upon P. cucumerina infection. Pharmacological inhibition of auxin transport or proteasome function each compromise necrotroph resistance of wild-type plants to a similar extent as in non-treated auxin response mutants. These results suggest that auxin signaling is important for resistance to the necrotrophic fungi P. cucumerina and B. cinerea. SGT1b (one of two Arabidopsis SGT1 genes encoding HSP90/HSC70 co-chaperones) promotes the functions of SCF E3-ubiquitin ligase complexes in auxin and JA responses and resistance conditioned by certain Resistance (R) genes to biotrophic pathogens. We find that sgt1b mutants are as resistant to P. cucumerina as wild-type plants. Conversely, auxin/SCF signaling mutants are uncompromised in RPP4-triggered resistance to the obligate biotrophic oomycete, Hyaloperonospora parasitica. Thus, the predominant action of SGT1b in R gene-conditioned resistance to oomycetes appears to be at a site other than assisting SCF E3-ubiquitin ligases. However, genetic additivity of sgt1b axr1 double mutants in susceptibility to H. parasitica suggests that SCF-mediated ubiquitination contributes to limiting biotrophic pathogen colonization once plant-pathogen compatibility is established.
authors.affiliation: Centro de Biotecnología y Genómica de Plantas (CBGP), Departamento de Biotecnología-UPM, ETS Ingenieros Agrónomos, Avda Complutense, E-28040 Madrid, Spain.
authors.forename: Francisco
authors.initials: F
authors.lastname: Llorente
authors.forename: Paul
authors.initials: P
authors.lastname: Muskett
authors.forename: Andrea
authors.initials: A
authors.lastname: Sánchez-Vallet
authors.forename: Gemma
authors.initials: G
authors.lastname: López
authors.forename: Brisa
authors.initials: B
authors.lastname: Ramos
authors.forename: Clara
authors.initials: C
authors.lastname: Sánchez-Rodríguez
authors.forename: Lucia
authors.initials: L
authors.lastname: Jordá
authors.forename: Jane
authors.initials: J
authors.lastname: Parker
authors.forename: Antonio
authors.initials: A
authors.lastname: Molina
mesh_terms: D017360:Arabidopsis / Q000187:drug effects / Q000235:genetics / Q000382:microbiology*; D029681:Arabidopsis Proteins / Q000502:physiology; D020171:Botrytis / Q000187:drug effects / Q000235:genetics / Q000472:pathogenicity*; D005658:Fungi / Q000187:drug effects / Q000472:pathogenicity*; D020022:Genetic Predisposition to Disease / Q000453:epidemiology*; D007113:Immunity, Innate / Q000502:physiology*; D007210:Indoleacetic Acids / Q000494:pharmacology*; D009154:Mutation; D010935:Plant Diseases / Q000382:microbiology*; D010937:Plant Growth Regulators / Q000494:pharmacology*; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology
chemical_list: C081977:AXR1 protein, Arabidopsis; D029681:Arabidopsis Proteins; D007210:Indoleacetic Acids; D010937:Plant Growth Regulators