The non-host pathogen Botrytis cinerea enhances glucose transport in Pinus pinaster suspension-cultured cells.

Botrytis cinerea is the causal agent of grey mould disease and a non-host necrotrophic pathogen of maritime pine (Pinus pinaster). Recent evidence suggests that pathogen challenge can alter carbon uptake in plant cells; however, little is known on how elicitor-derived signalling pathways control sugar transport activity. P. pinaster suspended cells are able to absorb D-[14C]glucose with high affinity, have an H+-dependent transport system (Km, 0.07 mM; Vmax, 1.5 nmol min(-1) mg(-1) DW), are specific for D-glucose, D-fructose, D-galactose and D-xylose, and are subject to glucose repression. When elicited by B. cinera spores, suspended cells exhibit calcium-dependent biphasic reactive oxygen species (ROS) production, the second burst also being dependent on NADPH oxidase, mitogen-activated protein kinase (MAPK), and de novo transcription and protein synthesis. Challenging suspended cells incubated in sugar-free medium resulted in an up to 3-fold increase in glucose transport capacity over non-elicited cultures 24 h after elicitation, and a 14-fold increase over elicited cells incubated with 2% glucose. Enhanced glucose uptake depended on NADPH oxidase and calcium influx, but not MAPK. In contrast, the increase of glucose transport activity induced by sugar starvation was dependent on the activation of MAPK but not NADPH oxidase. Both responses appeared to be dependent on de novo transcription and protein synthesis.