光是光合作用不可或缺的底物。然而过量的光照会对光合生物造成氧化胁迫和严重的损害。为了应对持续变化的光环境,蓝藻演化形成了灵活的电子传递网络。围绕光系统I(photosystem I,PSI)的循环电子传递(cyclic electron transport,CET)将...光是光合作用不可或缺的底物。然而过量的光照会对光合生物造成氧化胁迫和严重的损害。为了应对持续变化的光环境,蓝藻演化形成了灵活的电子传递网络。围绕光系统I(photosystem I,PSI)的循环电子传递(cyclic electron transport,CET)将电子从铁氧还蛋白Fd回流到质体醌(plastoquinone,PQ)库,产生ATP且不积累NADPH。在蓝藻和高等植物中发现了2种不同的CET途径,即NDH依赖途径和PGR5依赖途径。蓝藻中黄素二铁蛋白Flv1/Flv3参与了类梅勒(Mehler-like)反应,从PSI接受电子直接将氧气还原为水,且没有活性氧的形成。以集胞藻为试验材料,通过分析不同的CET和Flv突变株在不同光照条件下的生理特征以及其P700氧化/还原动力学,进而研究CET途径和类梅勒反应在集胞藻中的功能。结果表明NDH-1复合体对CET的贡献率超过90%,维持细胞能在持续高光环境下生长,而迅速应激的类梅勒反应在缓解瞬时高光胁迫时发挥了重要作用。因此我们认为在集胞藻中NDH-1介导的循环电子途径是稳固支持其适应高光逆境的主要机制,而类梅勒反应则是在现有主要途径严重不足时的1个备用途径。响应迅速的FLV路径是野生型和NDH-1突变株的补足。展开更多
The electron-transport machinery in photosynthetic membranes is known to be very sensitive to heat. In this study, the rate of electron transport (ETR) driven by photosystem I (PSI) and photosystem II (PSII) during he...The electron-transport machinery in photosynthetic membranes is known to be very sensitive to heat. In this study, the rate of electron transport (ETR) driven by photosystem I (PSI) and photosystem II (PSII) during heat stress in the wild-type Synechocystis sp. strain PCC 6803 (WT) and its ndh gene inactiva-tion mutants △ndhB (M55) and △ndhD1/ndhD2 (D1/D2) was simultaneously assessed by using the novel Dual-PAM-100 measuring system. The rate of electron transport driven by the photosystems (ETRPSs) in the WT, M55, and D1/D2 cells incubated at 30℃ and at 55℃ for 10 min was compared. Incubation at 55 ℃ for 10 min significantly inhibited PSII-driven ETR (ETRPSII) in the WT, M55 and D1/D2 cells, and the ex-tent of inhibition in both the M55 and D1/D2 cells was greater than that in the WT cells. Further, PSI-driven ETR (ETRPSI) was stimulated in both the WT and D1/D2 cells, and this rate was increased to a greater extent in the D1/D2 than in the WT cells. However, ETRPSI was considerably inhibited in the M55 cells. Analysis of the effect of heat stress on ETRPSs with regard to the alterations in the 2 active NDH-1 complexes in the WT, M55, and D1/D2 cells indicated that the active NDH-1 supercomplex and medi-umcomplex are essential for alleviating the heat-induced inhibition of ETRPSII and for accelerating the heat-induced stimulation of ETRPSI, respectively. Further, it is believed that these effects are most likely brought about by the electron transport mediated by each of these 2 active NDH-1 complexes.展开更多
基金Elite Youth Program of Chinese Academy of Agricultural Sciences and the Agricultural Science and Technology Innovation Program。
文摘光是光合作用不可或缺的底物。然而过量的光照会对光合生物造成氧化胁迫和严重的损害。为了应对持续变化的光环境,蓝藻演化形成了灵活的电子传递网络。围绕光系统I(photosystem I,PSI)的循环电子传递(cyclic electron transport,CET)将电子从铁氧还蛋白Fd回流到质体醌(plastoquinone,PQ)库,产生ATP且不积累NADPH。在蓝藻和高等植物中发现了2种不同的CET途径,即NDH依赖途径和PGR5依赖途径。蓝藻中黄素二铁蛋白Flv1/Flv3参与了类梅勒(Mehler-like)反应,从PSI接受电子直接将氧气还原为水,且没有活性氧的形成。以集胞藻为试验材料,通过分析不同的CET和Flv突变株在不同光照条件下的生理特征以及其P700氧化/还原动力学,进而研究CET途径和类梅勒反应在集胞藻中的功能。结果表明NDH-1复合体对CET的贡献率超过90%,维持细胞能在持续高光环境下生长,而迅速应激的类梅勒反应在缓解瞬时高光胁迫时发挥了重要作用。因此我们认为在集胞藻中NDH-1介导的循环电子途径是稳固支持其适应高光逆境的主要机制,而类梅勒反应则是在现有主要途径严重不足时的1个备用途径。响应迅速的FLV路径是野生型和NDH-1突变株的补足。
基金Supported by the National Natural Science Foundation of China (Grant No. 30770175)the Natural Science Foundation of Shanghai Muncipality (Grant No. 07ZR14086)+2 种基金the Innovation Program of Shanghai Municipal Education Commission (Grant No. 08ZZ67)the Key Foundation Project of Shanghai (Grant No. 06JC14091)the Leading Academic Discipline Project of Shanghai Municipal Education Commission (Grant No. J50401)
文摘The electron-transport machinery in photosynthetic membranes is known to be very sensitive to heat. In this study, the rate of electron transport (ETR) driven by photosystem I (PSI) and photosystem II (PSII) during heat stress in the wild-type Synechocystis sp. strain PCC 6803 (WT) and its ndh gene inactiva-tion mutants △ndhB (M55) and △ndhD1/ndhD2 (D1/D2) was simultaneously assessed by using the novel Dual-PAM-100 measuring system. The rate of electron transport driven by the photosystems (ETRPSs) in the WT, M55, and D1/D2 cells incubated at 30℃ and at 55℃ for 10 min was compared. Incubation at 55 ℃ for 10 min significantly inhibited PSII-driven ETR (ETRPSII) in the WT, M55 and D1/D2 cells, and the ex-tent of inhibition in both the M55 and D1/D2 cells was greater than that in the WT cells. Further, PSI-driven ETR (ETRPSI) was stimulated in both the WT and D1/D2 cells, and this rate was increased to a greater extent in the D1/D2 than in the WT cells. However, ETRPSI was considerably inhibited in the M55 cells. Analysis of the effect of heat stress on ETRPSs with regard to the alterations in the 2 active NDH-1 complexes in the WT, M55, and D1/D2 cells indicated that the active NDH-1 supercomplex and medi-umcomplex are essential for alleviating the heat-induced inhibition of ETRPSII and for accelerating the heat-induced stimulation of ETRPSI, respectively. Further, it is believed that these effects are most likely brought about by the electron transport mediated by each of these 2 active NDH-1 complexes.
