When tabtoxin was injected into Nicotiana tabacum leaves, glutamine synthetase was reduced by over 97% within 28 h, but the chlorotic and necrotic symptoms only occurred in illuminated leaves and were associated with the accumulation of ammonia. This indicated that symptom development was associated with accumulation of the substrate, rather than depletion of the product, of glutamine synthetase. Ammonia production by tabtoxin-treated tissue ceased immediately the tissue was darkened. A high carbon dioxide concentration and 3-(3,4-dichlorophenyl)-1-dimethyl urea (DCMU) also prevented ammonia production by such tissue. The ammonia was not derived from free pools of ammonia, amino acids or nitrate in the tissue, but was quantitatively accounted for by depletion of a fraction which would contain protein and polynucleotides. These results are consistent with the hypothesis that inhibition of glutamine synthetase by tabtoxin interrupts the photorespiratory-N cycle and the symptoms are associated with accumulation of an intermediate of this cycle, which is probably ammonia.