Publication details for Professor Marc KnightOkamoto, H, Gobel, C, Capper, RG, Saunders, N, Feussner, I & Knight, MR (2009). The alpha-subunit of the heterotrimeric G-protein affects jasmonate responses in Arabidopsis thaliana. Journal Of Experimental Botany 60(7): 1991-2003.
- Publication type: Journal papers: academic
- ISSN/ISBN: 0022-0957, 1460-2431
- DOI: 10.1093/jxb/erp060
- Keywords: AOS, Arabidopsis, Heterotrimeric G-protein, G-protein alpha-subunit (GPA1), Jasmonic acid, PDF1.2, VSP, Abscisic-acid, Methyl jasmonate, Beta-subunit, Transcription factor, Cell-proliferation, Disease resistance, Seed-germination, Coupled receptor.
- View online: Online version
- Durham research online: DRO record
Author(s) from Durham
Heterotrimeric G-proteins have been implicated in having a role in many plant signalling pathways. To understand further the role of G-proteins, a preliminary experiment was performed to assess the impact of the Gα subunit loss-of-function mutation gpa1-1 on the Arabidopsis transcriptome. The analysis indicated that the Gα subunit may play a role in response to jasmonic acid (JA). Consistent with this, Gα mutants showed a reduced response to JA in inhibition of chlorophyll accumulation and root growth, whilst Gα gain-of-function plants overexpressing Gα showed the opposite phenotype. The levels of JA and related compounds were unaffected in the gpa1-1 mutant, as was autoregulation of the Allene Oxide Synthase (AOS) gene that encodes a key enzyme for JA biosynthesis. In contrast, further analyses using Gα loss- and gain-of-function Arabidopsis lines indicated that Gα positively modulates the expression of the Vegetative Storage Protein (VSP) gene. This indicates that the Gα subunit regulates a subset of JA-regulated genes defining a branch point in this signalling pathway in Arabidopsis. Further analysis of the impact of Gα loss of function upon the JA-regulated transcriptome using Arabidopsis full genome arrays indicated that up to 29% of genes that are >2-fold regulated by JA in the wild type are misregulated in the Gα mutant. This supports the observation that a significant proportion of, but not all, JA-regulated gene expression is mediated by Gα.