Heterotrimeric G proteins-mediated resistance to necrotrophic pathogens includes mechanisms independent of salicylic acid-, jasmonic acid/ethylene- and abscisic acid-mediated defense signaling
| Autor: | Yuri, Trusov, Nasser, Sewelam, James Edward, Rookes, Matt, Kunkel, Ekaterina, Nowak, Peer Martin, Schenk, José Ramón, Botella |
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| Rok vydání: | 2008 |
| Předmět: |
Time Factors
Arabidopsis Proteins Basic Helix-Loop-Helix Leucine Zipper Transcription Factors GTP-Binding Protein beta Subunits Arabidopsis Alternaria Cyclopentanes Ethylenes Genes Plant Heterotrimeric GTP-Binding Proteins Defensins Plant Leaves Fusarium Host-Pathogen Interactions Mutation Oxylipins Salicylic Acid Abscisic Acid Disease Resistance Plant Diseases Signal Transduction |
| Zdroj: | The Plant journal : for cell and molecular biology. 58(1) |
| ISSN: | 1365-313X |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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