The response of electron transport mediated by active NADPH dehydrogenase complexes to heat stress in the cyanobacterium Synechocystis 6803
The response of electron transport mediated by active NADPH dehydrogenase complexes to heat stress in the cyanobacterium Synechocystis 6803
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蓝藻集胞藻 6803 中活性 NADPH 脱氢酶复合物介导的电子传递对热应激的响应
DOI：
10.1007/s11427-008-0139-0
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发表时间：
2008-12-01
期刊：
影响因子：
--
通讯作者：
Wang QuanXi
中科院分区：
文献类型：
--
作者：
Ma WeiMin;Wei LanZhen;Wang QuanXi
光合作用膜中的电子传递机制对热非常敏感。采用新型Dual-PAM-100测量系统，对集胞藻6803（WT）及其ndh基因失活突变体DeltandhB（M55）和DeltandhD 1/ndhD 2（D1/D2）在热胁迫下光系统I（PSI）和光系统II（PSII）驱动的电子传递速率（ETR）进行了同步测定。比较在30 ℃和55 ℃下孵育10分钟的WT、M55和D1/D2细胞中由光系统（ETR（PS））驱动的电子传递速率。在55 ℃下孵育10分钟显著抑制WT、M55和D1/D2细胞中PSII驱动的ETR（ETR（PSII）），并且M55和D1/D2细胞中的抑制程度均大于WT细胞中的抑制程度。此外，在WT和D1/D2细胞中均刺激了PSI驱动的ETR（ETR（PSI）），并且该速率在D1/D2中比在WT细胞中更大程度地增加。而在M55细胞中，ETR（PSI）被显著抑制。通过分析WT、M55和D1/D2细胞中2种活性NDH-1复合物的变化，发现活性NDH-1超复合物和中复合物分别对缓解热诱导的ETR抑制（PSII）和加速热诱导的ETR刺激（PSI）起重要作用。此外，据信这些作用最可能是由这2种活性NDH-1复合物中的每一种介导的电子传递引起的。
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 inactivation mutants DeltandhB (M55) and DeltandhD1/ndhD2 (D1/D2) was simultaneously assessed by using the novel Dual-PAM-100 measuring system. The rate of electron transport driven by the photosystems (ETR(PSs)) in the WT, M55, and D1/D2 cells incubated at 30 degrees C and at 55 degrees C for 10 min was compared. Incubation at 55 degrees C for 10 min significantly inhibited PSII-driven ETR (ETR(PSII)) in the WT, M55 and D1/D2 cells, and the extent of inhibition in both the M55 and D1/D2 cells was greater than that in the WT cells. Further, PSI-driven ETR (ETR(PSI)) 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, ETR(PSI) was considerably inhibited in the M55 cells. Analysis of the effect of heat stress on ETR(PSs) 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 mediumcomplex are essential for alleviating the heat-induced inhibition of ETR(PSII) and for accelerating the heat-induced stimulation of ETR(PSI), 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.