Heterotrimeric G proteins-mediated resistance to necrotrophic pathogens includes mechanisms independent of salicylic acid-, jasmonic acid/ethylene- and abscisic acid-mediated defense signaling

Trusov, Yuri, Sewelam, Nasser, Rookes, James Edward, Kunkel, Matt, Nowak, Ekaterina, Schenk, Peer Martin and Botella, Jose Ramon 2009, Heterotrimeric G proteins-mediated resistance to necrotrophic pathogens includes mechanisms independent of salicylic acid-, jasmonic acid/ethylene- and abscisic acid-mediated defense signaling, Plant journal, vol. 58, no. 1, pp. 69-81.

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Title 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, Jose Ramon
Journal name Plant journal
Volume number 58
Issue number 1
Start page 69
End page 81
Total pages 13
Publisher Wiley - Blackwell
Place of publication Malden, Mass.
Publication date 2009-04
ISSN 0960-7412
1365-313X
Keyword(s) plant biology
heterotrimeric G proteins
necrotrophic fungi
fusarium
arabidopsis
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.
Language eng
Field of Research 060799 Plant Biology not elsewhere classified
060199 Biochemistry and Cell Biology not elsewhere classified
Socio Economic Objective 829999 Plant Production and Plant Primary Products not elsewhere classified
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2008, Wiley-Blackwell Publishing
Persistent URL http://hdl.handle.net/10536/DRO/DU:30021304

Document type: Journal Article
Collection: School of Life and Environmental Sciences
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Created: Fri, 11 Dec 2009, 09:44:02 EST by Jim Rookes

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