Abstract
Sensitivity to photoinhibition under high light stress (2000 [mu]mol photons m-2 s-1 for 2 h in air) and recovery from this stress were examined in leaves of control, uninfected tobacco (Nicotiana tabacum cv Xanthi) leaves and in leaves in tobacco plants infected with tobacco mosaic virus (TMV) when grown under low light (150-200 [mu]mol photons m-2 s-1) or high light (1200 [mu]mol photons m-2 s-1) with high (8.0 mM) or low (0.5 mM) nitrate supply. Photoinhibition was monitored using the dark-adapted fluorescence parameters variable fluorescence/maximum fluorescence, an indicator of photosynthetic efficiency that correlated well with the quantum yield of photosynthetic oxygen evolution, and initial fluorescence, potentially an indicator of photoinhibitory damage. Susceptibility to photoinhibition was greater in low light- and low nitrogen-grown control plants than in high light- or high nitrogen-treated plants. Compared with uninfected controls, infection with the masked strain PV42 increased susceptibility to photoinhibition only in plants grown under low light/low nitrogen conditions. In expanding leaves, infection with severe strain TMV PV230 markedly accelerated photoinhibition under these conditions and under high light/low nitrogen conditions, even before visible symptoms were evident. High nitrogen levels during growth protected against this accelerated photoinhibitory response to virus infection during light stress and generally promoted recovery, at least prior to symptom development. As symptoms developed, the yellow regions provided evidence for chronic photoinhibitory damage, prior to and during the stress treatment, irrespective of growth conditions. Green regions of leaves showing visible symptoms were generally indistinguishable from control, uninfected plants during photoinhibitory stress and recovery. In developed leaves that remained free of visible symptoms during the experiments, in spite of the accumulation of about the same amounts of virus protein (S. Balachandran, C.B. Osmond, A. Makino [1994] Plant Physiol 104: 1043-1050) infection led to an acceleration of photoinhibition during stress treatments, especially in low light/low nitrogen treatments, in which chronic photoinhibitory damage was evident. These studies suggest a role for photoinhibitory damage in the acceleration of visible symptom development following TMV PV230 infection of expanding leaves, as well as in acceleration of senescence in developed leaves without visible symptoms.