Inhibition of photosynthesis in Nicotiana tabacum leaves treated with tabtoxin and its relation to pigment loss

Abstract

Tabtoxin is the chlorosis‐inducing dipeptide toxin produced by Pseudomonas syringae pv. tabaci, causal agent of the wildfire disease of Nicotiana tabacum L. cv. White Burley. In plant tissue it is hydrolysed to yield the amino acid tabtoxinine β‐lactam, which inactivates glutamine synthetase (EC 6.3.1.2). This study sought to identify those physiological alterations caused by the inactivation of glutamine synthetase and which were involved in the development of the chlorotic symptom. In tobacco (Nicotiana tabacum L. cv. White Burley) leaves injected with concentrations of taboxin that caused the inactivation of glutamine synthetase, photosynthesis was rapidly inhibited when the tissue was illuminated. This was closely followed by losses in leaf pigments, particularly chlorophyll a, and the ratio of chlorophyll a/b declined, indicating photochemical destruction. The rapid inhibition of photosynthesis in green tissue was due to reduced quantum efficiency, indicating a lesion in the light reactions. In chlorotic tissue, photosynthesis was limited by the chlorophyll level. The results indicated that the inhibition of photosynthesis may be instrumental in development of the chlorotic symptoms.