Inhibition of photosynthesis by Colletotrichum lindemuthianum in bean leaves determined by chlorophyll fluorescence imaging

• Published in: Plant, cell and environment Vol. 24; no. 9; pp. 947 - 956
• Main Authors: Meyer, S., Saccardy‐Adji, K., Rizza, F., Genty, B.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science, Ltd 01.09.2001; Blackwell; Wiley Subscription Services, Inc
• Subjects: anthracnose; Biological and medical sciences; Fundamental and applied biological sciences. Psychology; Fungal plant pathogens; gas exchange; Pathology, epidemiology, host-fungus relationships. Damages, economic importance; Phaseolus vulgaris; Phytopathology. Animal pests. Plant and forest protection; symptom assessment; Chlorophyll; Plant pathogen; Pathogenesis; Stomatal conductance; Fluorescence; Electron transfer; Host agent relation; Leaf area; Fungi; Grain legume; Leguminosae; Phaseolus vulgaris; Dicotyledones; Angiospermae; Colletotrichum lindemuthianum; Spermatophyta; Fungi Imperfecti; Gas exchange; Photosynthesis; Respiration; Thallophyta
• ISSN: 0140-7791; 1365-3040
• DOI: 10.1046/j.0016-8025.2001.00737.x

Infection of bean leaves by Colletotrichum lundemuthianum causes vein necrosis and subsequent localized wilting of the blade. The effect of infection on photosynthesis was investigated by imaging leaf chlorophyll fluorescence as a means of mapping stomatal and metabolic inhibition of photosynthesis. During infection, CO2 assimilation (An), stomatal conductance to water vapour, and photosynthetic electron transport rate (Jt) decreased, whereas dark respiration increased. An decreased more than was expected from the reduction in green leaf area, showing that photosynthesis was inhibited in apparently healthy areas. Under subsaturating irradiance, images of Jt in air showed that photosynthesis decreased gradually, with this effect shifting from green to necrotic areas. Sudden increase in CO2 concentration to 0·74% in the atmosphere around the leaf only partially reversed this inhibition, showing that both stomatal and metabolic inhibition occurred. Under limiting irradiance, decreases in Jt and in maximal Jt during high CO2 exposure as leaf damage severity increased suggested that metabolic inhibition was mediated through an inhibition of Ribulose 1·5‐bisphosphate (RuBP) regeneration. Finally, the importance of our data in terms of assessing the loss of photosynthetic yield from visible symptoms – as is currently performed in epidemiology – is discussed.