Heterotrimeric G proteins-mediated resistance to necrotrophic pathogens includes mechanisms independent of salicylic acid-, jasmonic acid/ethylene- and abscisic acid-mediated defense signaling.
Heterotrimeric G proteins are involved in the defense response against necrotrophic fungi in Arabidopsis. In order to elucidate the resistance mechanisms involving heterotrimeric G proteins, we analyzed the effects of the Gβ (subunit deficiency in the mutant agb1-2 on pathogenesis-related gene expression, as well as the genetic interaction between agb1-2 and a number of mutants of established defense pathways. Gβ-mediated signaling suppresses the induction of salicylic acid (SA)-, jasmonic acid (JA)-, ethylene (ET)- and abscisic acid (ABA)-dependent genes during the initial phase of the infection with Fusarium oxysporum (up to 48 h after inoculation). However, at a later phase it enhances JA/ET-dependent genes such as PDF1.2 and PR4. Quantification of the Fusarium wilt symptoms revealed that Gβ- and SA-deficient mutants were more susceptible than wild-type plants, whereas JA- and ET-insensitive and ABA-deficient mutants demonstrated various levels of resistance. Analysis of the double mutants showed that the Gβ-mediated resistance to F. oxysporum and Alternaria brassicicola was mostly independent of all of the previously mentioned pathways. However, the progressive decay of agb1-2 mutants was compensated by coi1-21 and jin1-9 mutations, suggesting that at this stage of F. oxysporum infection Gβ acts upstream of COI1 and ATMYC2 in JA signaling.
Trusov
Yuri
Y
School of Integrative Biology, University of Queensland, St. Lucia, Queensland, 4072, Australia.
Sewelam
Nasser
N
Rookes
James Edward
JE
Kunkel
Matt
M
Nowak
Ekaterina
E
Schenk
Peer Martin
PM
Botella
José Ramón
JR
D000040:Abscisic Acid / Q000235:genetics / Q000378:metabolism; D000528:Alternaria / Q000276:immunology / Q000472:pathogenicity; D017360:Arabidopsis / Q000235:genetics / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology; D029681:Arabidopsis Proteins / Q000235:genetics / Q000378:metabolism*; D051778:Basic Helix-Loop-Helix Leucine Zipper Transcription Factors / Q000235:genetics / Q000378:metabolism; D003517:Cyclopentanes / Q000378:metabolism; D023082:Defensins / Q000235:genetics / Q000378:metabolism; D060467:Disease Resistance; D005030:Ethylenes / Q000378:metabolism; D005670:Fusarium / Q000472:pathogenicity*; D044387:GTP-Binding Protein beta Subunits / Q000235:genetics / Q000378:metabolism; D017343:Genes, Plant; D020962:Heterotrimeric GTP-Binding Proteins / Q000235:genetics / Q000378:metabolism*; D054884:Host-Pathogen Interactions; D009154:Mutation; D054883:Oxylipins / Q000378:metabolism; D010935:Plant Diseases / Q000276:immunology / Q000382:microbiology; D018515:Plant Leaves / Q000235:genetics / Q000276:immunology / Q000382:microbiology; D020156:Salicylic Acid / Q000378:metabolism; D015398:Signal Transduction; D013997:Time Factors
D000040:Abscisic Acid; D029681:Arabidopsis Proteins; D051778:Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; D003517:Cyclopentanes; D023082:Defensins; D005030:Ethylenes; D044387:GTP-Binding Protein beta Subunits; D020962:Heterotrimeric GTP-Binding Proteins; D054883:Oxylipins; D020156:Salicylic Acid; C089590:AGB1 protein, Arabidopsis; C473611:MYC2 protein, Arabidopsis; C487542:At5g44420 protein, Arabidopsis; C011006:jasmonic acid; C036216:ethylene