Arabidopsis Heterotrimeric G-protein Regulates Cell Wall Defense and Resistance to Necrotrophic Fungi

DELGADO-CEREZO, M.; SÁNCHEZ-RODRÍGUEZ, C.; ESCUDERO, V.; MIEDES, E.; FERNÁNDEZ, PAULA VIRGINIA; JORDA, L.; HERNÁNDEZ-BLANCO, C.; SÁNCHEZ-VALET, A.; BEDNAREK, P.; SCHULZE-LEFER, P.; SOMERVILLE, S.; ESTEVEZ, JOSÉ MANUEL; PERSSON, S.; MOLINA, A.

MOLECULAR PLANT

OXFORD UNIV PRESS

Año: 2012 vol. 5 p. 98 - 114

1674-2052

The Arabidopsis heterotrimeric G protein controls defense responses to necrotrophic and vascular fungi. The agb1 mutant impaired in  the Gβ  subunit displays  enhanced susceptibility to  these  pathogens.  Gβ/AGB1 forms an obligate dimer with either one of the Arabidopsis Gγ  subunits (γ1/AGG1 and γ2/AGG2). Accordingly, we now demonstrate that the agg1 agg2 double mutant is as susceptible as  agb1  plants to the necrotrophic fungus  Plectosphaerella cucumerina. To elucidate the molecular basis of heterotrimeric G protein-mediated resistance, we performed a comparative transcriptomic analysis of agb1-1 mutant and wild-type plants upon inoculation with P. cucumerina. This analysis, together with metabolomic studies, demonstrated that G protein-mediated resistance was independent of defensive pathways required for resistance to necrotrophic fungi, such as the salicylic acid, jasmonic acid, ethylene, abscisic acid and tryptophan-derived metabolites signalling, as these pathways were not impaired in  agb1  and  agg1 agg2 mutants. Notably, many mis-regulated genes in agb1 plants were related with cell wall functions, which was also the case in  agg1 agg2  mutant. Biochemical analyses and Fourier Transform InfraRed (FTIR) spectroscopy of cell walls from G-protein mutants revealed that the xylose content was lower in agb1 and agg1 agg2 mutants than in wild-type plants, and that mutant walls had similar FTIR spectratypes, which differed from that of wild-type plants. The data presented here suggest a canonical functionality of the Gβ  and Gγ1/γ2 subunits in the control of Arabidopsis immune responses and the regulation of cell wall composition.