光胁迫下杂种杨无性系光合生理生态特征的研究

以气体交换测定结合合绿素荧光技术对几个杂种杨新无性系有自然光胁迫下的光合生理生态特性进行了分析。８月ＣＯ２气体交换测定显示,中午存在明显的光合作用下降现象,同时某些无性系午的气孔导度也有不同程度下降。叶绿素荧光分析显示,强光胁迫会影响光合作用的原初光反应过程,光系统Ⅱ（ＰＳⅡ）反应中心的最大光化学量子产率,有效光化学量子产率等反光系统Ⅱ反应中心活性的参数值在中午均比早晨低,与此同时,光系统Ⅱ反应中     

自然条件下珊瑚树（Viburnum odoratissimum）叶片光合作用的光抑制

利用气体交换观察、叶绿素荧光分析和ＱＢ蛋白含量的测定３种方法,研究了常绿灌木珊瑚树叶片的光合作用在上海深秋初冬自然条件下的光抑制,以便确定在除光以外不存在其它环境胁迫的自然条件下光合机构的破坏是否是引起光抑制的主要原因。经过中午３ｈ左右的强光照射以后,珊瑚树叶片的表观量子效率（ＡＱＹ）和ＰＳⅡ光化学效率（Ｆｖ／Ｆｍ）明显下降,表明珊瑚树叶在自然条件下经常发生光抑制。而且,经中午强光照射以后,叶片的初始荧光（Ｆ０）下降;非光化学荧光猝灭的慢弛豫成分（ｑＥｓｌｏｗ）上升;光饱和的光合速率略有下降;中午光照后降低了的ＡＱＹ和Ｆｖ／Ｆｍ在叶片离开强光１ｈ以后基本恢复;模拟中午光照的强光处理对叶片的ＱＢ蛋白含量没有明显的影响。这些事实都说明这种光抑制发生的主要原因是非光辐射能量耗散的增加,光合机构的破坏即使发生,也是很轻微的。     

青海高原及上海平原地区植物叶片光合作用的光抑制

用便携式ＡＤＣ光合气体分析系统和便携式ＣＦ－１０００荧光仪对青海和上海的同一植物和不同植物叶片光合作用的光抑制进行了测定。结果表明,两地在晴天强光下,中午植物叶片光系统Ⅱ（ＰＳⅡ）的光化学效率（Ｆｖ／Ｆｍ）和表观光合量子效率（ＡＱＹ）的日变化比早晨低;上海测定ＰＳⅡ的Ｆｖ／Ｆｍ和ＡＱＹ的日变化比青海的下降幅度大。ＡＱＹ的日变化曲线比ＰＳⅡ的Ｆｖ／Ｆｍ低,ＡＱＹ降低的幅度比ＰＳⅡ的Ｆｖ／Ｆｍ大。两地植物均有不同程度的光合作用光抑制,且上海比青海的大     

田间棉花叶片光合效率中午降低的原因

田间棉花叶片在受到中午强光或模拟的中午强光照射约３ｈ以后,光合效率和光系统Ⅱ的光化学效率（Ｆｖ／Ｆｍ）下降,光呼吸速率增加,并且普通空气条件下测定的光合效率的降低幅度总是大于Ｆｖ／Ｆｍ的降低幅度。然而,若抑制叶片的光呼吸,强光引起的叶片光合效率的降低幅度与Ｆｖ／Ｆｍ的基本一致。这些结果说明,光合作用的光抑制和光呼吸的增强是棉花叶片光合效率中午降低的两个基本原因。     

自然条件下珊瑚树叶片光合作用的光抑制

利用气体交换观察、叶绿素荧光分析和ＱＢ蛋白含量的测定３种方法,研究了常绿灌木珊瑚树叶片的光合作用在上海深秋初冬自然条件下的光抑制。以便确定在除光以外不存在其它环境胁迫的自然条件下光合机构的破坏是否时引起光抑制的主要原因。经过中午３ｈ左右的强光照射以后,珊瑚树叶片的表观量子效率和ＰＳⅡ光化学效率明显下降,表明珊瑚树叶在自然条件下经常发生光抑制。而且,经中午强光照射以后,叶片的初始荧光下降;非光化学荧     

田间小麦叶片光合作用的光抑制不伴随D1蛋白的净降解

通过测定田间小麦（Ｔｒｉｔｉｃｕｍ ａｅｓｔｉｖｕｍ ）叶片Ｄ１蛋白的含量、光合放氧和叶绿素ａ 荧光,探讨了叶片光合作用的光抑制与Ｄ１蛋白净降解的关系。田间的小麦叶片受到晴天中午光照约３ ｈ 以后,表观光合量子效率（Φ）、光系统Ⅱ的光化学效率（Ｆｖ／Ｆｍ ）和初始荧光（Ｆ０）明显下降;若将叶片转入弱光下,这３个指标可在１ ｈ 内基本恢复;强光照射过程中Ｄ１蛋白的含量没有显著变化;Ｄ１蛋白合成抑制剂ＳＭ 使强光下叶片的慢驰豫的非光化学荧光猝灭（ｑＥ－ｓｌｏｗ ）明显增加;在弱光下恢复时引入链霉素（ＳＭ）不影响叶片光合功能的恢复;用二硫苏糖醇（ＤＴＴ）抑制叶黄素循环使中午强光照射后的叶片中Ｄ１蛋白的含量降低３０％ 左右。这些结果都表明,田间小麦叶片光合作用的光抑制不是由于Ｄ１蛋白的净降解,而是由于非辐射能量耗散的增加引起的。     

杨梅光合作用的低温光抑制

利用便携式调制叶绿素荧光仪和光合作用测定系统研究了短期低温光照对杨梅幼树光合作用的影响。结果表明,低温光照处理后,杨梅叶片的Pn（净光合速率）、Gs（气孔导度）、Fv／Fm（最大的光系统Ⅱ光化学效率）、qP（光化学猝灭系数）和①PSⅡ（光系统Ⅱ的量子产量）下降,Ci／Ca（细胞间隙CO2浓度／环境CO2浓度）、Fo（初始荧光）、qN（非光化学猝灭系数）和（Fi—Fo）／（Fp—Fo）（失活的PSⅡ反应中心数量）上升。此外在同一水平低温下,中等强光（350μmol m^-2s^-1）加剧了PSⅡ反应中心的失活或破坏并且需要更长时间来恢复。这些结果说明低温和有光照条件下引起的杨梅光合作用下降是由于光合机构活性下降所致,即主要是PSⅡ反应中心的失活或破坏：我们推测QA^-（还原态质体醌A）和非还原QB（质体醌B）数量的积累可能是导致PSⅡ反应中心失活或破坏的原因,在低温光抑制过程中非辐射能量耗散对保护光合机构起着重要作用。     

水分胁迫对小麦旗叶某些体内叶绿素a荧光参数的影响

研究了水分胁迫对京冬６号品种小麦（ＴｒｉｔｉｃｕｍａｅｓｔｉｖｕｍＬ．）的旗叶（于杨花期）的体内（ｉｎｖｉｖｏ）叶绿素ａ荧光诱导动力学及几种叶绿素ａ荧光参数的影响,以探究水分胁迫损伤光合作用的机理。通过将离体叶片放置于干燥器中不同时间以得到三种干旱的情况（失水叶片的ＲＷＣ分别为５０．９％,３１．５％和１７．５％。对照叶片的ＲＷＣ为７３．５％）。体内叶绿素ａ荧光特性是用ＰＡＭ叶绿素荧光计测定的。我们观察到水分胁迫显著地改变了小麦旗叶的重复饱和光脉冲激发的调制叶绿素ａ荧光诱导动力学的图形。对从这种荧光动力学的实验数据得到的四种重要的体内叶绿素ａ荧光参数：Ｆｍ／Ｆｏ值（最大荧光与基础荧光的比值）、（ｇ－ｈ）值（饱和光脉冲诱导的荧光尖峰信号高度）、ｑＰ值（光化学淬灭系数）和ｑＮ值（非光化学淬灭系数）,水分胁迫都有抑低的作用。并且我们注意到,在水分胁迫的严重程度与这四种荧光参数被抑低的程度之间,存在着正相关关系。我们的实验数据指出,水分胁迫抑制了光系统Ⅱ的氧化侧,并且也降低了光合膜的能量化作用     

模拟酸雨对龙眼叶片气体交换和叶绿素a荧光参数的影响（英文）

 研究了模拟酸雨对龙眼(Dimorcarpus longana)叶片气体交换和叶绿素a荧光参数的影响,结果表明：酸雨胁迫抑制龙眼光合作用,受胁迫叶片光补偿点上升。pH 3.0的酸雨处理6 h后叶片气体交换和叶绿素a荧光参数下降,停止处理后72 h可以恢复。pH 2.5的酸雨处理6 h后净光合速率（Pn）、气孔导度(Cs)、蒸腾速率（Tr）,叶绿素a荧光参数Fv/Fo、Fv/Fm、PSII非环式电子传递的量子产量（ΦPSⅡ）、荧光下降比值（Rfd）、非光化学猝灭系数（qN）和光化学猝灭系数（qP）急剧下降,停     

中午强光胁迫下高蛋白小麦旗叶的光合特性

测定了大田种植条件下４ 个不同籽粒蛋白质含量小麦品系旗叶的净光合作用、光呼吸作用和荧光参数的日变化以及旗叶功能期内ＰＳⅡ光化学效率的变化。结果表明：高、低蛋白小麦旗叶的净光合速率无显著差异,但中午强光胁迫下高蛋白小麦ＰＳⅡ光化学效率（Ｆｖ／Ｆｍ） 较高,ＰＳⅡＦｖ／Ｆｍ 下降得较少,而净光合速率午间下降的幅度较大,原因可能是高蛋白小麦品系旗叶内氮素代谢活动旺盛（ 其代谢限速酶硝酸还原酶活性显著高于低蛋白品种） ,光呼吸作用较强,从而消耗了较多的过剩激发能,在一定程度上减轻了Ｆｖ／Ｆｍ 的下降,而较强的光呼吸作用同时降低了光合速率     

CO2 response of cyclic electron flow around PSI (CEF-PSI) in tobacco leaves--relative electron fluxes through PSI and PSII determine the magnitude of non-photochemical quenching (NPQ) of Chl fluorescence

We hypothesized that cyclic electron flow around photosystem I (CEF-PSI) participates in the induction of non-photochemical quenching (NPQ) of chlorophyll (Chl) fluorescence when the rate of photosynthetic linear electron flow (LEF) is electron-acceptor limited. To test this hypothesis, the relationships among photosynthesis rate, electron fluxes through both PSI and PSII [Je(PSI) and Je(PSII)] and Chl fluorescence parameters were analyzed simultaneously in intact leaves of tobacco plants at several light intensities and partial pressures of ambient CO2 (Ca). At low light intensities, decreasing Ca lowered the photosynthesis rate, but Je(PSI) and Je(PSII) remained constant. Je(PSI) was larger than Je(PSII), indicating the existence of CEF-PSI. Increasing the light intensity enhanced photosynthesis and both Je(PSI) and Je (PSII). Je(PSI)/Je(PSII) also increased at high light and at high light and low Ca combined, showing a strong, positive relationship with NPQ of Chl fluorescence. These results indicated that CEF-PSI contributed to the dissipation of photon energy in excess of that consumed by photosynthesis by driving NPQ of Chl fluorescence. The main physiological function of CEF-PSI in photosynthesis of higher plants is discussed.     

Two-step mechanism of photodamage to photosystem II: step 1 occurs at the oxygen-evolving complex and step 2 occurs at the photochemical reaction center

Under strong light, photosystem II (PSII) of oxygenic photosynthetic organisms is inactivated, and this phenomenon is called photoinhibition. In a widely accepted model, photoinhibition is induced by excess light energy, which is absorbed by chlorophyll but not utilized in photosynthesis. Using monochromatic light from the Okazaki Large Spectrograph and thylakoid membranes from Thermosynechococcus elongatus, we observed that UV and blue light inactivated the oxygen-evolving complex much faster than the photochemical reaction center of PSII. These observations suggested that the light-induced damage was associated with a UV- and blue light-absorbing center in the oxygen-evolving complex of PSII. The action spectrum of the primary event in photodamage to PSII revealed the strong effects of UV and blue light and differed considerably from the absorption spectra of chlorophyll and thylakoid membranes. By contrast to the photoinduced inactivation of the oxygen-evolving complex in untreated thylakoid membranes, red light efficiently induced inactivation of the PSII reaction center in Tris-treated thylakoid membranes, and the action spectrum resembled the absorption spectrum of chlorophyll. Our observations suggest that photodamage to PSII occurs in two steps. Step 1 is the light-induced inactivation of the oxygen-evolving complex. Step 2, occurring after step 1 is complete, is the inactivation of the PSII reaction center by light absorbed by chlorophyll. We confirmed our model by illumination of untreated thylakoid membranes with blue and UV light, which inactivated the oxygen-evolving complex, and then with red light, which inactivated the photochemical reaction center.     

PHOTOSYNTHETIC RESPONSE OF THE GIANT KELP MACROCYSTIS PYRIFERA (PHAEOPHYCEAE) TO ULTRAVIOLET RADIATION1

Solar ultraviolet radiation (UVA + UVB) impairs photosynthesis in marine algae. Canopy blades of the giant kelp Macrocystis pyrifera (L.) C. Agardh are exposed to high levels of solar UV in the field. To determine the effects of UV radiation on photosynthesis in the giant kelp and to identify sites of UV damage, O₂ evolution, reaction center organization, light harvesting, and energy transfer efficiency were measured in canopy blades that had been exposed to elevated levels of UV in the laboratory. UV treatment reduced both the light-saturated rate and the light-limited rate of photosynthesis by 50% but produced no significant change in the rate of dark respiration. A significant impairment of photosystem II (PSII) reaction center function was observed, suggesting that PSII is a major site of damage in chromophytes. Reduced quantum efficiency of photosynthesis and loss of energy transfer from light-harvesting pigments (fucoxanthin, chlorophyll a, and chlorophyll c) to PSII indicate that the major light-harvesting complex of M. pyrifera, the fucoxanthin-chlorophyll protein complex (FCPC), was another site of UV damage. These measures provide the first evidence of a direct effect of UV radiation on specific sites in the photosynthetic apparatus of chromophytes and indicate that in situ fluorescence excitation analysis may be a simple means to detect UV stress in algae.     

PGRL1 overexpression in Phaeodactylum tricornutum inhibits growth and reduces apparent PSII activity

Proton gradient regulation 5‐like photosynthetic phenotype 1 (PGRL1)‐dependent cyclic electron transport around photosystem I (PSI) plays important roles in the response to different stresses, including high light. Although the function of PGRL1 in higher plants and green algae has been thoroughly investigated, little information is available on the molecular mechanism of PGRL1 in diatoms. We created PGRL1 overexpression and knockdown transformants of Phaeodactylum tricornutum, the diatom model species, and investigated the impact on growth and photosynthesis under constant and fluctuating light conditions. PGRL1 over‐accumulation resulted in significant decreases in growth rate and apparent photosystem II (PSII) activity and led to an opposing change of apparent PSII activity when turning to high light, demonstrating a similar influence on photosynthesis as a PSII inhibitor. Our results suggested that PGRL1 overexpression can reduce the apparent efficiency of PSII and inhibit growth in P. tricornutum. These findings provide physiological evidence that the accumulation of PGRL1 mainly functions around PSII instead of PSI.     

C_3植物光合效率的日变化

多种田间C_3植物在晴天的光合效率常有明显的日变化,中午前后光合效率降低。C_3植物大豆叶片光合效率中午降低的主要原因,不是空气CO_2浓度和气孔导度及光呼吸的变化,而可能是光抑制。因为:1.在饱和CO_2中测定仍可观测到这种中午降低;2.光合作用的饱和光强远低于晴天中午的太阳光强;3.用纱布预遮阴可以提高叶片的光合效率;4.阴天时叶片光合效率不发生中午降低。     

Responses to desiccation stress in bryophytes and an important role of dithiothreitol-insensitive non-photochemical quenching against photoinhibition in dehydrated states

The effects of air drying and hypertonic treatments in the dark on seven bryophytes, which had grown under different water environments, were studied. All the desiccation-tolerant species tested lost most of their PSII photochemical activity when photosynthetic electron transport was inhibited by air drying, while, in all the sensitive species, the PSII photochemical activity remained at a high level even when photosynthesis was totally inhibited. The PSI reaction center remained active under drying conditions in both sensitive and tolerant species, but the activity became non-detectable in the light only in tolerant species due to deactivation of the cyclic electron flow around PSI and of the back reaction in PSI. Light-induced non-photochemical quenching (NPQ) was found to be induced not only by the xanthophyll cycle but also by a DeltapH-induced, dithiothreitol-insensitive mechanism in both the desiccation-tolerant and -intolerant bryophytes. Both mechanisms are thought to have an important role in protecting desiccation-tolerant species from photoinhibition under drying conditions. Fluorescence emission spectra at 77K showed that dehydration-induced quenching of PSII fluorescence was observed only in tolerant species and was due to neither state 1-state 2 transition nor detachment of light-harvesting chlorophyll protein complexes from PSII core complexes.The presence of dehydration-induced quenching of PSI fluorescence was also suggested.     

Very strong UV-A light temporally separates the photoinhibition of photosystem II into light-induced inactivation and repair

When organisms that perform oxygenic photosynthesis are exposed to strong visible or UV light, inactivation of photosystem II (PSII) occurs. However, such organisms are able rapidly to repair the photoinactivated PSII. The phenomenon of photoinactivation and repair is known as photoinhibition. Under normal laboratory conditions, the rate of repair is similar to or faster than the rate of photoinactivation, preventing the detailed analysis of photoinactivation and repair as separate processes. We report here that, using strong UV-A light from a laser, we were able to analyze separately the photoinactivation and repair of photosystem II in the cyanobacterium Synechocystis sp. PCC 6803. Very strong UV-A light at 364 nm and a photon flux density of 2600 micromol photons m(-2) s(-1) inactivated the oxygen-evolving machinery and the photochemical reaction center of PSII within 1 or 2 min before the first step in the repair process, namely, the degradation of the D1 protein, occurred. During subsequent incubation of cells in weak visible light, the activity of PSII recovered fully within 30 min and this process depended on protein synthesis. During subsequent incubation of cells in darkness for 60 min, the D1 protein of the photoinactivated PSII was degraded. Further incubation in weak visible light resulted in the rapid restoration of the activity of PSII. These observations suggest that very strong UV-A light is a useful tool for the analysis of the repair of PSII after photoinactivation.     

FIRST INDUCED PLASTID GENOME MUTATIONS IN AN ALGA WITH SECONDARY PLASTIDS: psbA MUTATIONS IN THE DIATOM PHAEODACTYLUM TRICORNUTUM (BACILLARIOPHYCEAE) REVEAL CONSEQUENCES ON THE REGULATION OF PHOTOSYNTHESIS1

Diatoms play a crucial role in the biochemistry and ecology of most aquatic ecosystems, especially because of their high photosynthetic productivity. They often have to cope with a fluctuating light climate and a punctuated exposure to excess light, which can be harmful for photosynthesis. To gain insight into the regulation of photosynthesis in diatoms, we generated and studied mutants of the diatom Phaeodactylum tricornutum Bohlin carrying functionally altered versions of the plastidic psbA gene encoding the D1 protein of the PSII reaction center (PSII RC). All analyzed mutants feature an amino acid substitution in the vicinity of the Q_B‐binding pocket of D1. We characterized the photosynthetic capacity of the mutants in comparison to wildtype cells, focusing on the way they regulate their photochemistry as a function of light intensity. The results show that the mutations resulted in constitutive changes of PSII electron transport rates. The extent of the impairment varies between mutants depending on the proximity of the mutation to the Q_B‐binding pocket and/or to the nonheme iron within the PSII RC. The effects of the mutations described here for P. tricornutum are similar to effects in cyanobacteria and green microalgae, emphasizing the conservation of the D1 protein structure among photosynthetic organisms of different evolutionary origins.     

Cytochrome b-559 may function to protect photosystem II from photoinhibition

Although cytochrome b-559 is an integral component of the photosystem II complex (PSII), its function is unknown. Because cytochrome b-559 has been shown to be both photooxidized and photoreduced in PSII, one of several proposals is that it mediates cyclic electron transfer around PSII, possibly as a protective mechanism. We have used electron paramagnetic resonance spectroscopy to investigate the pathway of photooxidation of cytochrome b-559 in PSII and have shown that it proceeds via photooxidation of chlorophyll. We propose that this photooxidation of chlorophyll is the first step in the photoinhibition of PSII. The unique susceptibility of PSII to photoinhibition is probably due to the fact that it is the only reaction center in photosynthesis which generates an oxidant with a reduction potential high enough to oxidize chlorophyll. We propose that the function of cytochrome b-559 is to mediate cyclic electron transfer to rereduce photooxidized chlorophyll and protect PSII from photoinhibition. We also suggest that the chlorophyll(s) which are susceptible to photooxidation are analogous to the monomer chlorophylls found in the bacterial photosynthetic reaction center complex.     

Very strong UV-A light temporally separates the photoinhibition of photosystem II into light-induced inactivation and repair

When organisms that perform oxygenic photosynthesis are exposed to strong visible or UV light, inactivation of photosystem II (PSII) occurs. However, such organisms are able rapidly to repair the photoinactivated PSII. The phenomenon of photoinactivation and repair is known as photoinhibition. Under normal laboratory conditions, the rate of repair is similar to or faster than the rate of photoinactivation, preventing the detailed analysis of photoinactivation and repair as separate processes. We report here that, using strong UV-A light from a laser, we were able to analyze separately the photoinactivation and repair of photosystem II in the cyanobacterium Synechocystis sp. PCC 6803. Very strong UV-A light at 364 nm and a photon flux density of 2600 μmol photons m⁻² s⁻¹ inactivated the oxygen-evolving machinery and the photochemical reaction center of PSII within 1 or 2 min before the first step in the repair process, namely, the degradation of the D1 protein, occurred. During subsequent incubation of cells in weak visible light, the activity of PSII recovered fully within 30 min and this process depended on protein synthesis. During subsequent incubation of cells in darkness for 60 min, the D1 protein of the photoinactivated PSII was degraded. Further incubation in weak visible light resulted in the rapid restoration of the activity of PSII. These observations suggest that very strong UV-A light is a useful tool for the analysis of the repair of PSII after photoinactivation.