Short-term responses of photosystem I to heat stress - Induction of a PS II-independent electron transport through PS I fed by stromal components

Short-term responses of photosystem I to heat stress - Induction of a PS II-independent electron transport through PS I fed by stromal components
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DOI:
10.1007/bf00017756
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发表时间:
1996-01-01
影响因子:
3.7
通讯作者:
Havaux, M
Havaux, M
中科院分区:
生物学3区
文献类型:
--
作者:
Havaux, M

文献摘要

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当23摄氏度生长的马铃薯叶(Solanum tuberosum L.)在弱光下暴露于高温15分钟,在高于约38 ℃的温度下观察到光系统(PS)II的显著和优先失活。体内光声测量表明,伴随着PS II活性的丧失,热应激诱导了仅激发PS I的远红光(>715 nm)和激发PS I和PS II的宽带光(350-600 nm)的显著气体摄取活性。鉴于其抑制氮气和氧气和高二氧化碳浓度的刺激,大部分的光声测量的气体吸收热应激叶片归因于快速的二氧化碳溶解响应光调制基质碱化耦合PS I驱动的电子传递。观察到热诱导的气体吸收对PS II抑制剂敌草隆不敏感,对质体蓝素抑制剂HgCl 2敏感,并且在约1200 μ E m(-2)s(-1)的相当高的光子通量密度下饱和。当从远红光过渡到黑暗时,PS I的氧化反应中心P700(+)在对照叶片中非常缓慢地被再还原(半衰期t(1/2)高于500 ms),如通过叶片在820 nm附近的吸光度变化所测量的。热胁迫引起了显着的加速光照后P700(+)的减少,与t(1/2)下降到低于50毫秒的值(叶片暴露于48摄氏度后)。降低的t(1/2)对氯化汞敏感,对敌草隆、甲基紫精(PS I的电子受体,与内源受体铁氧还蛋白竞争)和厌氧不敏感。这种P700(+)还原的加速是由热处理(在不到5分钟内)引起的,即使在用远红光长时间照射叶片后也能持续。热胁迫后,质体醌池表现出减少在黑暗中的叶绿素荧光的表观Fo水平的增加,可以被远红光淬灭所示。应用程序(1分钟)的远红光热预处理的叶子也诱导可逆淬灭的最大荧光水平Fm,这表明在远红光形成的pH梯度。两者合计,所提出的数据表明,PS I响应热诱导的PS II光化学活性的损失,通过催化基质还原剂的电子流。热应激诱导的PS I电子传递不依赖于PS II,似乎构成了一种保护机制,因为观察到缺氧条件下该电子途径的阻断会导致PS I的显着光失活。
When 23 degrees C-grown potato leaves (Solanum tuberosum L.) were exposed for 15 min to elevated temperatures in weak light, a dramatic and preferential inactivation of Photosystem (PS) II was observed at temperatures higher than about 38 degrees C. In vivo photoacoustic measurements indicated that, concomitantly with the loss of PS II activity, heat stress induced a marked gas-uptake activity both in far-red light (>715 nm) exciting only PS I and in broadband light (350-600 nm) exciting PS I and PS II. In view of its suppression by nitrogen gas and oxygen and its stimulation by high carbon-dioxide concentrations, the bulk of the photoacoustically measured gas uptake by heat-stressed leaves was ascribed to rapid carbon-dioxide solubilization in response to light-modulated stroma alkalization coupled to PS I-driven electron transport. Heat-induced gas uptake was observed to be insensitive to the PS II inhibitor diuron, sensitive to the plastocyanin inhibitor HgCl2 and saturated at a rather high photon flux density of around 1200 mu E m(-2) s(-1). Upon transition from far-red light to darkness, the oxidized reaction center P700(+) of PS I was re-reduced m very slowly in control leaves (with a half time t(1/2) higher than 500 ms), as measured by leaf absorbance changes at around 820 nm. Heat stress caused a spectacular acceleration of the postillumination P700(+) reduction, with t(1/2) falling to a value lower than 50 ms (after leaf exposure to 48 degrees C). The decreased t(1/2) was sensitive to HgCl2 and insensitive to diuron, methyl viologen (an electron acceptor of PS I competing with the endogenous acceptor ferredoxin) and anaerobiosis. This acceleration of the P700(+) reduction was very rapidly induced by heat treatment (within less than 5 min) and persisted even after prolonged irradiation of the leaves with far-red light. After heat stress, the plastoquinone pool exhibited reduction in darkness as indicated by the increase in the apparent Fo level of chlorophyll fluorescence which could be quenched by far-red light. Application (for 1 min) of far-red light to heat-pretreated leaves also induced a reversible quenching of the maximal fluorescence level Fm, suggesting formation of a pH gradient in far-red light. Taken together, the presented data indicate that PS I responded to the heat-induced loss of PS II photochemical activity by catalyzing an electron flow from stromal reductants. Heat-stress-induced PS I electron transport independent of PS II seems to constitute a protective mechanism since block of this electron pathway in anaerobiosis was observed to result in a dramatic photoinactivation of PS I.