Scaling of photosynthesis and constitutive and induced volatile emissions with severity of leaf infection by rust fungus (Melampsora larici-populina) in Populus balsamifera var. suaveolens.
Fungal infections result in decreases in photosynthesis, induction of stress and signaling volatile emissions and reductions in constitutive volatile emissions, but the way different physiological processes scale with the severity of infection is poorly known. We studied the effects of infection by the obligate biotrophic fungal pathogen Melampsora larici-populina Kleb., the causal agent of poplar leaf rust disease, on photosynthetic characteristics, and constitutive isoprene and induced volatile emissions in leaves of Populus balsamifera var. suaveolens (Fisch.) Loudon. exhibiting different degrees of damage. The degree of fungal damage, quantified by the total area of chlorotic and necrotic leaf areas, varied between 0 (noninfected control) and ∼60%. The rates of all physiological processes scaled quantitatively with the degree of visual damage, but the scaling with damage severity was weaker for photosynthetic characteristics than for constitutive and induced volatile release. Over the whole range of damage severity, the net assimilation rate per area (AA) decreased 1.5-fold, dry mass per unit area 2.4-fold and constitutive isoprene emissions 5-fold, while stomatal conductance increased 1.9-fold and dark respiration rate 1.6-fold. The emissions of key stress and signaling volatiles (methanol, green leaf volatiles, monoterpenes, sesquiterpenes and methyl salicylate) were in most cases nondetectable in noninfested leaves, and increased strongly with increasing the spread of infection. The moderate reduction in AA resulted from the loss of photosynthetically active biomass, but the reduction in constitutive isoprene emissions and the increase in induced volatile emissions primarily reflected changes in the activities of corresponding biochemical pathways. Although all physiological alterations in fungal-infected leaves occurred in a stress severity-dependent manner, modifications in primary and secondary metabolic pathways scaled differently due to contrasting operational mechanisms.