条锈病对小麦（Triticum aestivum L.）叶片光合功能及光合功能蛋白D1表达的影响

测定了小麦（Triticum aestivum L.）感染小麦条锈病后的光合常数,以及叶绿素含量、类囊体膜光合电子传递速率和光合反应中心D1蛋白的变化。实验显示,条锈病侵染导致感病小麦叶片净光合速率与叶绿素含量降低;抗病小麦经侵染后净光合速率却有恢复过程,叶绿素含量先降后升。此外,感病小麦叶片被侵染后全链电子传递速率受到抑制,PSII电子传递速率的变化与全链电子传递速率的变化趋势相似,但PSI电子传递速率受到的影响较小;抗病小麦小麦叶片被侵染后电子传递速率所受影响较小。同时发现,病程中,感病和抗病小麦PSII的光合反应中心D1蛋白含量变化总是与PSII电子传递速率的变化类似,推测D1蛋白的表达量变化是引起PSII电子传递活性与全链电子传递速率变化的主要因素之一。     

外源Ca2＋对高温强光胁迫下灌浆期小麦叶片光合机构运转的影响

灌浆期叶面喷施10mmol·L-1 CaCl2对高温强光胁迫下小麦叶片光合电子传递、放氧速率、叶绿素荧光参数和D1蛋白的影响结果表明,Ca2＋预处理可保护D1蛋白,削弱其降解,提高光系统I（PSI）和光系统Ⅱ（PSⅡ）子传递速率、全链电子传递速率、净光合速率（Pn）、PSII最大光化学效率（Fv/Fm）、PSII实际光化学效率（ΦPSⅡ）和光化学猝灭（qp）,维持较低的Fo,最终导致小麦适应高温强光的能力提高。     

苹果褐斑病菌侵染对苹果叶片光合机构功能的影响

为了探究苹果褐斑病菌侵染对苹果叶片光合机构的伤害机制,以‘寒富’苹果为试材,研究苹果褐斑病菌侵染对苹果叶片光合作用和光系统功能的影响。结果表明：随褐斑病菌侵染加重（叶片感病程度分0、1、2、3、4和5级）,叶片的叶绿素a含量和总叶绿素含量持续下降,其中2～5级与对照相比差异显著,病菌侵染提高了叶片类胡萝卜素含量,但仅以2级与对照差异显著。苹果褐斑病菌侵染显著降低了叶片的净光合速率（Pn）,3～5级病叶的Pn分别较对照下降44．9％、56．6％和70．3％,而胞间CO2浓度（Ci）上升,说明非气孔因素是光合作用的主要限制因子。褐斑病菌侵柒影响了光合电子传递效率,随病菌侵染程度加重,光系统Ⅱ反应中心、供体侧放氧复合体（Wk）和受体侧（Vj）受到的伤害加重,并引起苹果叶片PSII的光合性能指数用PIABS和PSI受体侧末端电子受体的量子产额（φRo）急剧下降。褐斑病菌侵染加重了苹果叶片的膜脂过氧化程度,1～5级感病叶片的丙二醛（MDA）含量均显著高于对照,引发超氧化物歧化酶（SOD）及过氧化物酶（POD）活性的上调。以上结果表明,苹果褐斑病菌侵染引起叶片光合色素降解,对PSII反应中心、受体侧和供体侧造成伤害,进一步影响了PSI的电子传递效率,并导致叶片膜脂过氧化,造成苹果叶片光合能力下降。     

光强度对小麦幼苗光合特性的影响

研究了在两种不同光强下水培5－7天的小麦（Triticum aestivum)“农大139”幼苗的光合特性,观察到生长期间的不同光强度对麦幼苗的光合膜一些成分和光合特性有明显影响,单位叶面积或单位鲜重中的Chl含量,Chl a/b比值,单位鲜重中的Car含量,以及光合膜中CPIa和CPI的含量,在低光强（2×10^3lx)下生长的幼苗都低,而光合膜中的LHCP的含量则高于在高光强（2×10^4lx)下生长的小麦幼苗,荧光诱导动力学测定结果表明,在高光强下生长的小麦其光合单位较小,而PSII活性和PSII原初光能转化效率都较高,同时,它们的叶绿体的PSII,PSI和全链电子传递速率也较高。     

D,L-甘油醛处理引起的小麦叶片表观光合量子效率的降低（英文）

D,L-甘油醛(磷酸核酮糖激酶抑制剂,10mmol/L)处理小麦旗叶1 h可降低叶片净光合速率和表观量子效率.同时,光系统Ⅱ光化学效率(△F/Fm′)、电子传递速率(ETR)和单位叶面积ATP含量均降低,而胞间二氧化碳浓度(Ci)和叶绿素荧光非光化学猝灭(NPQ)增加.这些结果说明,D,L-甘油醛引起的小麦旗叶表观量子效率降低是由于光合碳同化受阻对光合电子传递的反馈抑制.     

外源Ca2+对高温强光胁迫下小麦叶绿体D1蛋白磷酸化及光系统Ⅱ功能的影响

用10 mmol·L^-1 CaCl₂溶液预处理灌浆期小麦叶片,以水预处理为对照,然后将预处理植株进行高温强光（35 ℃,1600 μmol·m^-2·s^-1）胁迫,测定胁迫处理过程中小麦旗叶光合电子传递速率、净光合速率、叶绿素荧光参数及D₁蛋白的变化,以研究外源Ca²⁺对高温强光胁迫下小麦叶片类囊体膜D₁蛋白磷酸化和PSⅡ功能的影响.结果表明：CaCl₂溶液预处理使小麦叶片在高温强光逆境下PSⅡ反应中心发生可逆失活,有效抑制了高温强光下D₁蛋白的净降解,保持了较高的D₁蛋白磷酸化水平,暗恢复后PSⅡ反应中心活性迅速恢复,全链电子传递速率和PSⅡ电子传递速率恢复至对照水平,维持了较高的PSⅡ原初光化学效率（F_v/F_m）、实际光化学效率(Ф_PSⅡ)、光化学猝灭系数（q_P）和净光合速率（P_n）.表明外源Ca²⁺通过调节小麦叶绿体D₁蛋白的周转,促进了PSⅡ的正常运转,减轻了高温强光胁迫对叶片光合机构的损伤.     

水杨酸对高温强光胁迫下小麦叶绿体D1蛋白磷酸化及光系统Ⅱ功能的影响

为了研究水杨酸（SA）对高温强光胁迫下小麦叶片类囊体膜D₁蛋白磷酸化和PSⅡ功能的影响,用0.5 mmol·L^-1 SA溶液预处理灌浆期小麦叶片,以水预处理为对照,然后将预处理植株进行高温强光（35 ℃,1 600 μmol·m^-2·s^-1）处理,测定胁迫处理过程中小麦旗叶光合电子传递速率、净光合速率、叶绿素荧光参数及D₁蛋白的变化.结果表明：SA预处理有效抑制了高温强光下D₁蛋白的净降解,保持了较高的D₁蛋白磷酸化水平、全链电子传递速率和PSⅡ电子传递速率,维持了较高的PSⅡ原初光化学效率（F_v/F_m）、实际光化学效率(Ф_PSⅡ)、光化学淬灭系数（q_P）和净光合速率（P_n）.表明外源SA通过调节小麦叶绿体D₁蛋白的周转,减轻了高温强光胁迫对叶片光合机构的损伤,有利于PSⅡ的正常运转.     

施氮和大气CO2浓度升高对小麦旗叶光合电子传递和分配的影响

采用开顶式气室盆栽培养小麦,设计2个大气CO2浓度(正常:400 μmol.mol-1;高:760 μmol·mol-1)、2个氮素水平(0和200 mg·kg-1土)的组合处理,通过测定小麦抽穗期旗叶氮素和叶绿素浓度、光合速率(Pn)-胞间CO2浓度(C1)响应曲线及荧光动力学参数,来测算小麦叶片光合电子传递速率等,研究了高大气CO2浓度下施氮对小麦旗叶光合能量分配的影响.结果表明:与正常大气CO2浓度相比,高大气CO2浓度下小麦叶片氮浓度和叶绿素浓度降低,高氮处理的小麦叶片叶绿素a/b升高.施氮后小麦叶片PSⅡ最大光化学效率(Fv/Fm)、PSⅡ反应中心最大量子产额(Fv'/Fm')、PSⅡ反应中心的开放比例(qr)和PSⅡ反应中心实际光化学效率(φPSⅡ)在大气CO2浓度升高后无明显变化,虽然叶片非光化学猝灭系数(NPQ)显著降低,但PSⅡ总电子传递速率(JF)无明显增加;不施氮处理的Fv'/Fm'、φPSⅡ和NPQ在高大气CO2浓度下显著降低,尽管Fv/Fm和qp无明显变化,JF仍显著下降.施氮后小麦叶片JF增加,参与光化学反应的非环式电子流传递速率(Jc)明显升高.大气CO2浓度升高使参与光呼吸的非环式电子流传递速率(J0)、Rubisco氧化速率(V0)、光合电子的光呼吸/光化学传递速率比(J0/Jc)和Rubisco氧化/羧化比(V0/Vc)降低,但使Jc和Rubisco羧化速率(Vc)增加.因此,高大气CO2浓度下小麦叶片氮浓度和叶绿素浓度降低,而增施氮素使通过PSⅡ反应中心的电子流速率显著增加,促进了光合电子流向光化学方向的传递,使更多的电子进入Rubisco羧化过程,Pn显著升高.     

外源硅对纹枯病菌(Rhizoctonia solani)侵染下水稻叶片光合功能的改善

为了进一步探讨外源加硅增强水稻对纹枯病的抗性作用,以抗病品种91SP和感病品种Lemont为材料,研究了人工接种纹枯病菌条件下外源硅对水稻叶片叶绿素含量、光合作用、叶绿素荧光特性和MDA含量的影响。结果表明：（1）外源加硅能降低抗病品种91SP的纹枯病病级和病情指数,显著降低感病品种Lemont的病级和病情指数;（2）接种纹枯病菌后,水稻叶片叶绿素含量、净光合速率（Pn）、气孔导度（Gs）均明显降低,胞间CO2浓度（Ci）增大,而加硅处理的水稻叶片叶绿素含量、Pn、Gs不同程度增加,Ci有所降低;（3）接种纹枯病菌后,两个品种PSⅡ最大光化学效率（Fv／Fm）、PSⅡ有效光化学效率（Fv＇／Fm＇）、PSⅡ实际光化学效率（ФPSⅡ）、光化学猝灭系数（qP）和表观光合电子传递速率（ETR）均降低,非光化学猝灭系数（qNP）增大,而对于加硅处理的水稻叶片,上述荧光参数在纹枯病菌侵染条件下的变化均受到不同程度的抑制。（4）外源硅可不同程度地减缓纹枯病菌侵染引起的丙二醛（MDA）含量的增加,对感病品种Lemont的缓解作用要大于抗病品种91SP。可见,外源硅处理可以不同程度地缓解纹枯病菌侵染条件下非气孔因素引起的水稻叶片光合速率的下降以及对光合机构的破坏作用,提高光化学效率,改善叶片的光合功能,减轻叶片膜脂过氧化程度,增强水稻对纹枯病的抗性。     

D，L—甘油醛处理引起的小麦叶片表观光合量子效率的降低

D,L－甘油醛（磷酸核酮糖激酶抑制剂,10mmol/L)处理小麦旗叶1h可降低叶片净光合速率和表观量子效率。同时,光系统Ⅱ光化学效率（ΔF/Fm′）,电子传递速率（ETR）和单位叶面积ATP含量均降低,而胞间二氧化碳浓度（Ci)和叶绿素荧光非光化学猝灭（NPQ）增加,这些结果说明,D,L－甘油醛引起的小麦旗叶表观量子效率降低是由于光合碳同化受阻对光合电子传递的反馈抑制。     

两种高产小麦旗叶光合功能衰退特性的比较

以高产小麦宁麦8号和9号为材料,研究了自开花期旗叶光合功能衰退和品种间的差异。结果表明:开花期后,随着穗重的增加,旗叶的比叶重、相对含水量、叶绿素含量、饱和光强下的净光合速率P_nmax、光饱和点LSP、表观量子产量AQY以及PSI、PS II和全电子传递链活性不断降低,黄熟期后下降均较显著,而叶绿素a/b、光补偿点LCP和呼吸速率R_d开花期至黄熟期间缓慢升高。和宁麦8号相比,宁麦9号叶绿素含量开始时较低,衰老后期含量较高。结论:黄熟期前,旗叶对光的利用范围较光,光合功能降低缓慢;黄熟期后,利用强光和弱光能力均下降,光合功能的衰退显著。和宁麦8号相比,高产小麦宁麦9号旗叶光合功能早衰。     

Drought-induced changes in chlorophyll fluorescence,photosynthetic pigments,and thylakoid membrane proteins of Vigna radiata

The effects of drought on chlorophyll fluorescence characteristics of PSII, photosynthetic pigments, thylakoid membrane protein (D1), and proline content in different varieties of mung bean plants were studied. Drought stress inhibits PSII activity and induces alterations in D1 protein. We observed a greater decline in the effective quantum yield of PSII, electron transport rate, and saturating photosynthetically active photon flux density (PPFD_sat) under drought stress in var. Anand than var. K-851 and var. RMG 268. This may possibly be due to either downregulation of photosynthesis or photoinhibition process. Withholding irrigation resulted in gradual diminution in total Chl content at Day 4 of stress. HPLC analysis revealed that the quantity of β-carotene in stressed plants was always higher reaching maxima at Day 4. Photoinactivation of PSII in var. Anand includes the loss of the D1 protein, probably from greater photosynthetic damage caused by drought stress than the other two varieties.     

不同盐胁迫下小麦叶片渗透性调节和叶绿素荧光特性

盐胁迫对植物伤害机理受到普遍关注。本试验以‘西旱3号’小麦幼苗为材料,通过比较钠盐(150 mmol·L^-1)、钙盐(5、30 mmol·L^-1)单独及其复合胁迫对叶片渗透调节和光合特性的影响,揭示不同盐胁迫对小麦的伤害机理。结果表明: 钠盐或钙盐单独胁迫显著抑制了小麦幼苗根、茎的生长,使叶片可溶性糖和脯氨酸含量、调节性能量耗散电子产量、非光化学猝灭及玉米黄质相对含量均显著增加,而叶绿素a和叶绿素b含量、最大光化学效率、PSⅡ实际光化学效率、光化学猝灭及光合电子传递效率均显著下降。此外,钙盐对小麦幼苗生长的抑制作用更强,钠盐处理下叶片叶绿素含量减少和叶绿素荧光参数降低更显著。除了可溶性蛋白、叶黄素和玉米黄质相对含量以外,低浓度钙盐有效缓解了钠盐诱导其他各指标的变化,而高浓度钙盐进一步增大了钠盐处理小麦幼苗各参数的变化幅度。总之,钠盐和钙盐显著抑制了小麦幼苗的生长,低浓度钙盐能有效缓解钠盐对小麦幼苗的伤害,而高浓度钙盐加剧了钠盐的毒害作用。这均与叶片光合色素含量、光能捕获及光合电子传递的改变有关。此外,渗透调节物质在增强钠盐或钙盐环境中小麦幼苗的抗性方面发挥着重要作用。     

Stress-induced degradation of the photosynthetic apparatus is accompanied by changes in thylakoid protein turnover and phosphorylation

Development of chlorosis and loss of PSII were compared in young spinach plants suffering under a combined magnesium and sulphur deficiency. Loss of chlorophyll could be detected already after the first week of deficiency and preceded any permanent functional inhibition of PSII as detected by changes in the chlorophyll fluorescence parameter F_v/F_m. A substantial decrease in F_v/F_m was observed only after the second week of deficiency. After 4 weeks, the plants had lost about 70% of their original chlorophyll content, but fluorescence data indicated that 80% of the existing PSII centers were still capable of initiating photosynthetic electron transport. The degradation of the photosynthetic apparatus without loss of PSII activity was due to changes in protein turnover, especially of the PSII D1 reaction center protein. Already by day 7 of deficiency, a 1.4-fold increase in D1 protein synthesis was observed measured as incorporation of ¹⁴C-leucine. Immunological determination by western-blotting did not reveal a change in D1 protein content. Thus, D1 protein was also degraded more rapidly. The increased turnover was high enough to prevent any loss or inhibition of PSII. After 3 weeks, D1 protein synthesis on a chlorophyll basis was further increased by a factor of 2. However, this was not enough to prevent a net loss of D1 protein of about 70%. Immunological determination revealed that together with the D1 protein also other polypeptides of PSII became degraded. This process prevented a large accumulation of photo-inactivated PSII centers. However, it initiated the breakdown of the other thylakoid proteins, especially of LHCII, resulting in the observed chlorosis. Together with the change in protein turnover and stability, a characteristic change in thylakoid protein phosphorylation was observed. In the deficient plants steady state phosphorylation of both LHCII and PSII proteins was increased in the dark. In the light phosphorylation of PSII proteins was stimulated and after 3 weeks of deficiency was even higher in the deficient leaves than in the control plants. In contrast, the phosphorylation level of LHCII decreased in the light and could hardly be detected after 3 weeks of deficiency. Phosphorylation of the reaction center polypeptides presumably increased their stability against proteolytic attack, whereas phosphorylated LHCII seems to be the substrate for proteolysis.     

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.     

Effect of Reducing Nitric Oxide in <Emphasis Type="Italic">Rumex</Emphasis> K-1 Leaves on the Photoprotection of Photosystem II Under High Temperature with Strong Light

The purpose of this study was to explore the effect of reducing nitric oxide (NO) in Rumex K-1 leaves on the photoprotection of photosystem II (PSII) under high temperature with strong light. Reducing the content of NO in Rumex K-1 leaves significantly aggravated the PSII photoinhibition and net degradation of D1 protein under high temperature with strong light, but not under high temperature in the darkness. The reduction of NO remarkably inhibited the electron transport of PSII in the leaves under high temperature and strong light, which resulted in an increase in excitation pressure and an over-accumulation of reactive oxygen species (ROS). The over-accumulation of ROS further damaged PSII. However, when the synthesis of D1 protein was inhibited, the D1 protein content and PSII activity were no longer influenced by reducing NO content in the leaves. The reduction of NO in leaves decreased the activities of ROS scavenger enzymes after treatment with high temperature and strong light for 2 h, which enhanced the over-accumulation of ROS to damage photosynthetic apparatus severely. All of these results suggest that NO was involved in the synthesis of D1 protein. Maintaining physiologically appropriate NO content in leaves will alleviate net degradation of D1 protein under high temperature with strong light to keep photosynthetic electrons flowing smoothly, which mitigates the accumulation of ROS in photosystems to avoid damage to the photosynthetic apparatus. Therefore, NO plays an important role in maintaining higher PSII photosynthetic performance under high temperature with strong light.     

The effects of excess manganese on photosynthetic rate and concentration of chlorophyll in Triticum aestivum grown in solution culture

Manganese toxicity, which involves a broad array of physiological responses, has been identified as an important factor limiting plant growth on acid soils. In the experiments reported here, we examined the toxic effects of Mn on chlorophyll content, photosynthesis and respiration in two cultivars (Norquay and Columbus) of Triticum aestivum (wheat) which differ in tolerance of Mn. When grown over a range of concentrations of Mn (0–1 000 μ M ), the Mn-tolerant cultivar maintained higher rates of photosynthesis and respiration, and higher concentrations of chlorophyll a and chlorophyll b , than did the Mn-sensitive cultivar, despite greater accumulations of Mn in leaf tissues. After 5 days growth with 1 000 μ M Mn in solution, the photosynthetic rate fell to 25% of control in the sensitive cultivar and to only 75% of control in the tolerant cultivar. The concentration of chlorophyll a fell to 50% of control in the sensitive cultivar, but did not differ from control in the tolerant cultivar. Greater effects were seen on concentrations of chlorophyll b . which fell to 35% and 55% of control in the sensitive and tolerant cultivars, respectively. Rates of photosynthesis decreased in both cultivars as concentrations of chlorophyll decreased; however, the photosynthetic rate per unit chlorophyll remained constant or increased in the tolerant cultivar and decreased in the sensitive cultivar as concentrations of Mn in solution increased. Thus, in the sensitive cv. Columbus, Mn seemed to have a toxic effect on both chlorophyll content and photosynthesis per unit chlorophyll. In the tolerant cv. Norquay, the only clear effect of Mn was a reduction in chlorophyll content, although direct inhibition of photosynthesis could not be discounted.