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Heterotrimeric G proteins‐mediated resistance to necrotrophic pathogens includes mechanisms independent of salicylic acid‐, jasmonic acid/ethylene‐ and abscisic acid‐mediated defense signaling
Author(s) -
Trusov Yuri,
Sewelam Nasser,
Rookes James Edward,
Kunkel Matt,
Nowak Ekaterina,
Schenk Peer Martin,
Botella José Ramón
Publication year - 2009
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2008.03755.x
Subject(s) - jasmonic acid , heterotrimeric g protein , abscisic acid , salicylic acid , alternaria brassicicola , mutant , biology , fusarium oxysporum , arabidopsis , signal transduction , microbiology and biotechnology , biochemistry , gene , g protein , botany
Summary 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.