SummaryThe kinetics of ion efflux from leaf discs were used to show that there is no general increase in the permeability of plasmalemma or tonoplast resulting from infection of barley leaves by brown rust (Puccinia hordei Otth.). An assay of in vivo chlorophyll fluorescence showed that there were clear differences between chloroplasts in healthy and diseased tissue, but overall the thylakoid lamellae function well in rusted barley leaves. We conclude that in this biotrophic system there is no gross impairment of host membrane integrity, and show that delivery of host nutrients to the apoplast is at rates greatly in excess of those needed to accommodate fungal nutrient uptake. This does not preclude localized effects of the pathogen on host membranes.

SummaryThe movement of 32P, fractionation of 32P and unlabelled phosphorus, and efflux of 32P from leaf discs, in control and brown‐rust infected first leaf blades of barley are described for the day of sporulation, 7 d after infection. It is shown that P retranslocation is greatly reduced by disease, that the concentration of P in the infected leaf blade increases greatly and that the increase is probably largely in the fungus, and partly in the form of polyphosphate. The P content of fungal spores is derived largely from P currently entering the leaf in the xylem. The data are used to derive P budgets for control and infected leaf‐blades, and the significance of P to the diseased state is discussed.

The rate of net photosynthesis is reduced in leaves of barley infected with brown rust. This reduction is not due to reduced carbon dioxide fixation per chloroplast, but is ascribed to a decrease in the number of functional chloroplasts. Chloroplasts isolated from diseased leaves show increased contents of starch and phosphorus, and unaltered rates of ferricyanide-dependent oxygen evolution, as compared with controls. Fluxes through the phosphate translocator on the chloroplast inner envelope are shown to be higher in diseased leaves. The kinetics of in vivo chlorophyll fluorescence induction are described, and it is shown that whilst they change with leaf age in control leaves, in diseased leaves the juvenile kinetics are retained. These data are interpreted as showing that each surviving chloroplast in diseased leaves is functioning at least as well as those from healthy leaves.

Levels of calcium, magnesium, potassium, nitrogen and phosphorus have been measured in young barley plants with the first leaf infected with brown rust. The rate of uptake per unit of root was increased by disease for the cations and nitrogen but not for phosphorus. In infected leaves, potassium and phosphorus accumulated to above control levels. The behaviour of the cations can be entirely explained by relatively unaltered xylem import into diseased leaves, but reduced export of the phloem-mobile ions. Nitrogen and phosphorus show more complex behaviour. Nitrogen import into infected leaves was increased, whilst the increased level of phosphorus in diseased leaves is explicable by reduced retranslocation coupled with active accumulation within the infected leaf blade.