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 <i>agb1-2</i> on pathogenesis-related gene expression, as well as the genetic interaction between <i>agb1-2</i> 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 <i>Fusarium oxysporum</i> (up to 48 h after inoculation). However, at a later phase it enhances JA/ET-dependent genes such as <i>PDF1.2</i> and <i>PR4</i>. 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 <i>F. oxysporum</i> and <i>Alternaria brassicicola</i> was mostly independent of all of the previously mentioned pathways. However, the progressive decay of <i>agb1-2</i> mutants was compensated by <i>coi1-21</i> and<i> jin1-9</i> mutations, suggesting that at this stage of <i>F. oxysporum</i> infection Gβ acts upstream of COI1 and ATMYC2 in JA signaling.<br />