Role of ammonium accumulation in bacteria‐induced hypersensitive and compatible reactions of tobacco and cotton plants

Abstract

Leaves of 12‐week‐old tobacco plants (Nicotiana tabacum L. cv. Samsun NN) were infiltrated with suspensions of Pseudomonas syringae pv, pisi (DSM 50291) to induce hypersensitive reaction (HR). Cotyledons of 2‐week‐old cotton plants (Gossypium hirsutum L. cv. Acala 442 and Coker BR) were infiltrated with Xanthomonas campestris pv. malvacearum (race 10) to induce the disease. In tobacco, HR‐related increases in NH+4 levels started within 2 h after infection and continued up to the time of tissue decay. Increase of NH+4 and especially K+ efflux were detected in intercellular washing fluids (IWF). Antibiotics stopped and later reverted NH+4 production and K+ efflux, but only if applied within 2 h after infection. When 10 mM NH+4 was injected into leaves, it was rapidly consumed from the IWF, and also, although more slowly, within the leaf cells. The concomitant K+ efflux was strong but delayed, and most of the K+ was reabsorbed after 2 h. Bacterial cell multiplication in HR stopped before the appearance of HR symptoms and cell necrosis. In the compatible reaction in cotton cotyledons, both NH+4accumulation and K+ efflux proceeded much more slowly than in the HR with tobacco, and bacteria continued to multiply until general cell necrosis occurred. The compatible reaction developed faster in constant darkness than in a light/dark rhythm. Bacterial enzymes produced NH+4, mainly from proteins of host cells, in both light and darkness. Continuous light delayed the main peak of both NH+4 production and K+ efflux. High CO2 concentration inhibited both processes, thus indicating that photorespiration plays a role in enhancing the release of free ammonium during bacterial pathogenesis. This is supported by shifts in the pattern of amino acids. The results demonstrate the accelerating and aggravating effect of ammonium in pathogenesis and HR, though ammonium is not the primary agent.