Plants of the discovered chlorophyll-deficient mutant of oak (ML) display enhanced disease resistance to the fungus Erysiphe cichoracearum, causal agent of powdery mildew. Quantitative imaging of chlorophyll (Chl) fluorescence revealed that the net photosynthetic rate (PN) declined progressively in both untreated and invaded ML leaves as well as in inoculated wild-type (WT) leaves. Images of non-photochemical fluorescence quenching (NPQ) in both untreated and infected mutant leaves suggested that the capacity of Calvin cycle had been reduced and that there was a complex metabolic heterogeneity within the ML leaf. The ML mutant accumulates reactive oxygen species, ROS (H2O2) from the oxidative burst followed by spontaneous cell death that mimic the hypersensitive response. Reduction in pathogen sporulation on ML leaves correlated with the accumulation of soluble saccharides and a more rapid induction of defence responses including expression of some defence proteins (β-1,3-glucanase and chitinase). Unlike to WT plants, ML- conferred phenotype activates and/or de-represses multiple defence responses, making them more easily induced by pathogens.