Matthijs Hans C P, Jeanjean Robert, Yeremenko Nataliya, Huisman Jef, Joset Francoise, Hellingwerf Klaas J
Institute for Biodiversity and Ecosystem Dynamics/Aquatic Microbiology, Faculty of Science, University of Amsterdam, Nieuwe Achtergracht 127, 1018WS Amsterdam, The Netherlands.Corresponding author; email:
Laboratoire de ChimLaboratoire de Chimie Bacterienne/Centre National de Recherche Scientifique, 31 Chemin Joseph Aiguier, 13402 Marseille Cedex 20, France.
Funct Plant Biol. 2002 Apr;29(3):201-210. doi: 10.1071/PP01197.
Pseudo-reversion of the high-CO2 requiring phenotype of the NADH dehydrogenase type 1-impaired mutant of Synechocystis PCC6803, strain M55, by salt stress coincides with partial restoration of PSI-driven cyclic electron transfer. In M55, the complete family of D proteins (D1-D6) that are needed for electron transfer through the complex is lacking. Adaptation to salt stress requires de novo synthesis of full-length 47-kDa ferredoxin-NADP reductase (FNR). A mutant created in the M55 background, which only expresses truncated chloroplast 37-kDa FNR cannot adapt to salt stress and refrains from growth in low CO2. A special feature of FNR in cyanobacteria is the relatively high molecular mass of 44-48 kDa. A positively charged extended N-terminal domain of the cyanobacterial enzyme defines the extra mass. The extension likely plays a key role in the salt-stress inducible enhancement of PSI-driven cyclic electron transfer, and in the pseudo-reversion of the high-CO2 requiring phenotype of M55. Data acquired with several other cyanobacteria and the oxychlorobacterium Prochlorothrix hollandica contributed to the present hypothesis. It proposes that FNR is involved in regulation of inducible and transient PSI cyclic electron transfer in cyanobacteria via a thylakoid surface charge and conditional-proteolysis steered mechanism.
盐胁迫导致集胞藻PCC6803的1型NADH脱氢酶受损突变体M55的高二氧化碳需求表型发生假回复，这与光系统I驱动的循环电子传递的部分恢复相吻合。在M55中，缺乏通过该复合体进行电子传递所需的完整D蛋白家族（D1-D6）。适应盐胁迫需要从头合成全长47 kDa的铁氧还蛋白-NADP还原酶（FNR）。在M55背景下创建的一个突变体，其仅表达截短的叶绿体37 kDa FNR，无法适应盐胁迫，并且在低二氧化碳条件下无法生长。蓝细菌中FNR的一个特殊特征是相对较高的分子量，为44-48 kDa。蓝细菌酶带正电荷的延伸N端结构域决定了额外的质量。该延伸可能在盐胁迫诱导的光系统I驱动的循环电子传递增强以及M55的高二氧化碳需求表型的假回复中起关键作用。从其他几种蓝细菌和嗜氧绿菌荷兰原绿球藻获得的数据支持了本假设。该假设提出，FNR通过类囊体表面电荷和条件性蛋白水解调控机制参与蓝细菌中诱导性和瞬时性光系统I循环电子传递的调节。
