Balachandran S., Osmond C. B.
Department of Botany, Duke University, Durham, North Carolina 27708.
Plant Physiol. 1994 Mar;104(3):1051-1057. doi: 10.1104/pp.104.3.1051.
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.
研究了在高光胁迫（空气中2000 μmol光子·m⁻²·s⁻¹，持续2小时）下对照、未感染烟草（烟草品种Xanthi）叶片以及感染烟草花叶病毒（TMV）的烟草植株叶片对光抑制的敏感性及其从该胁迫中的恢复情况。这些烟草植株在低光（150 - 200 μmol光子·m⁻²·s⁻¹）或高光（1200 μmol光子·m⁻²·s⁻¹）条件下生长，并分别供应高（8.0 mM）或低（0.5 mM）硝酸盐。使用暗适应荧光参数可变荧光/最大荧光来监测光抑制，该参数是光合效率的指标，与光合放氧的量子产率相关性良好，同时监测初始荧光，其可能是光抑制损伤的指标。在低光和低氮条件下生长的对照植株比高光或高氮处理的植株对光抑制更敏感。与未感染的对照相比，感染隐性株系PV42仅在低光/低氮条件下生长的植株中增加了对光抑制的敏感性。在伸展叶中，感染强毒株TMV PV230在这些条件下以及高光/低氮条件下显著加速了光抑制，甚至在可见症状出现之前就已如此。生长期间的高氮水平可防止在光胁迫期间病毒感染导致的这种加速光抑制反应，并通常促进恢复，至少在症状出现之前如此。随着症状的发展，黄色区域显示在胁迫处理之前和期间存在慢性光抑制损伤，与生长条件无关。在实验期间未出现可见症状的成熟叶中，尽管积累了大致相同量的病毒蛋白（S. Balachandran、C.B. Osmond、A. Makino [1994] Plant Physiol 104: 1043 - 1050），但感染在胁迫处理期间导致光抑制加速，特别是在低光/低氮处理中，其中慢性光抑制损伤明显。这些研究表明，光抑制损伤在TMV PV230感染伸展叶后可见症状发展的加速过程中起作用，以及在无可见症状的成熟叶衰老加速过程中起作用。
