Thimann K V, Tetley R M, Krivak B M
The Thimann Laboratories, Division of Natural Sciences, University of California, Santa Cruz, California 95064.
Plant Physiol. 1977 Mar;59(3):448-54. doi: 10.1104/pp.59.3.448.
A comparison has been made of the progress of senescence in the first leaf of 7-day-old oat plants (Avena sativa cv. Victory) in darkness and in white light. Light delays the senescence, and intensities not over 100 to 200 ft-c (1000-2000 lux) suffice for the maximum effect. In such intensities, chlorophyll loss and amino acid liberation still go on in detached leaves at one-third to one-half the rate observed in darkness; however, when the leaves are attached to the plant, the loss of chlorophyll in 5 days is barely detectable. Transfer of the leaves from 1 or 2 days in the low intensity light to darkness, or vice versa, shows no carryover of the effects of the preceding exposure, so that such treatment affords no evidence for the photoproduction of a stable substance, such as cytokinin, inhibiting senescence. Light causes a large increase in invertaselabile sugar and a smaller increase in glucose, and application of 100 to 300 mm glucose or sucrose in the dark maintains the chlorophyll, at least partially. Correspondingly, short exposure to high light intensity, which increased the sugar content, had a moderate effect in maintaining the chlorophyll. However, 3-(3,4-dichlorphenyl)-1,1-dimethylurea (DCMU) completely prevents the increases in sugars and yet does not prevent the effect of light on senescence, whether determined by chlorophyll loss or by protein hydrolysis. Light causes a 300% increase in the respiration of detached oat leaves, and kinetin lowers that only partly, but unlike the increased respiration associated with senescence in the dark, the increase in the light is fully sensitive to dinitrophenol, and therefore cannot be ascribed to respiratory uncoupling. The increased respiration in light is prevented by DCMU, parallel with the prevention of sugar formation. It is therefore ascribed to the accumulation of soluble sugars, acting as respirable substrate. Also, l-serine does not antagonize the light effect. For all of these reasons, it is concluded that the action of light is not mediated by photosynthetic sugar formation, nor by photoproduction of a cytokinin. Instead, we propose that light exerts its effect by photoproduction of ATP. The action of sugars is ascribed to the same mechanism but by way of respiratory ATP. This hypothesis unifies most of the observed phenomena of the senescence process in oat leaves, and helps to explain some of the divergent findings of earlier workers.
对7日龄燕麦植株（燕麦品种Victory）第一片叶子在黑暗和白光条件下的衰老进程进行了比较。光照会延缓衰老，强度不超过100至200英尺烛光（1000 - 2000勒克斯）即可产生最大效果。在这种强度下，离体叶片中叶绿素的损失和氨基酸的释放仍以在黑暗中观察到的速率的三分之一至二分之一进行；然而，当叶片与植株相连时，5天内叶绿素的损失几乎检测不到。将叶片在低强度光照下放置1或2天后转移至黑暗中，反之亦然，结果表明先前光照的影响没有残留，因此这种处理无法为光产生抑制衰老的稳定物质（如细胞分裂素）提供证据。光照会使转化酶易分解糖大幅增加，葡萄糖增加幅度较小，在黑暗中施加100至300毫摩尔的葡萄糖或蔗糖至少能部分维持叶绿素含量。相应地，短时间暴露于高光强度下，这会增加糖含量，对维持叶绿素也有一定作用。然而，3 -（3,4 - 二氯苯基）-1,1 - 二甲基脲（DCMU）完全阻止了糖含量的增加，但无论是通过叶绿素损失还是蛋白质水解来判断，都不能阻止光照对衰老的影响。光照会使离体燕麦叶片的呼吸作用增加300%，激动素只能部分降低其呼吸作用，但与黑暗中与衰老相关的呼吸作用增加不同，光照下的呼吸作用增加对二硝基苯酚完全敏感，因此不能归因于呼吸解偶联。DCMU可阻止光照下呼吸作用的增加，同时也阻止了糖的形成。因此，这归因于可溶性糖的积累，作为可呼吸的底物。此外，L - 丝氨酸不会拮抗光照的作用。基于所有这些原因，得出结论：光照的作用不是通过光合糖的形成介导的，也不是通过细胞分裂素的光产生介导的。相反，我们提出光照通过光产生ATP发挥作用。糖的作用归因于相同的机制，但通过呼吸ATP。这一假设统一了燕麦叶片衰老过程中观察到的大多数现象，并有助于解释早期研究者的一些不同发现。
