When leaves of Nicotiana tabacum L. var. Xanthi were inoculated with TMV, local lesion formation gave enhanced ATP concentration accompanied by increased respiration. Phosphorus metabolism in healthy and infected leaves was investigated either by floating leaf tissue on 32P1-phosphate buffer or by allowing intact leaves to take up 32P1-phosphate buffer through the petioles. Both methods gave increased 32P1 incorporation into inorganic and organic acid-soluble phosphorus fractions of the infected leaf. Comparison of the specific activity of 32P1-phosphate buffer supplied with the specific activity of the γ-phosphate group of ATP demonstrated that 50 per cent of the ATP in the healthy leaf compared with over 78 per cent of the ATP in the infected leaf was metabolically active in respiration. As the ATP concentration in the infected leaf is much greater than that in the healthy leaf, this means that the amount of ATP being utilized and resynthesized as a result of respiratory metabolism in the infected leaf is more than twice that in the healthy leaf. Pulse-labelling experiments demonstrated that the rate of ATP turnover was very similar in healthy and infected leaves; therefore the increased respiration in the infected leaf results from the larger ATP pool with a turnover rate of ATP similar to that in the healthy leaf. With tobacco callus tissue cultures infected by TMV, where infection does not result in local-lesion formation, phosphorus metabolism was unaltered in the infected tissue. It is concluded that necrotic local-lesion formation results from increased availability of ATP at sites of ATP utilization, and this is aggravated by over-production of ATP in the infected leaf.
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Merrett et al. (1969) studied this question.
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