controlofhydrogenphotoproductionbytheprotongradientgeneratedbycyclicelectronflow阅读笔记

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1、ControlofhydrogenphotoproductionbytheprotongradientgeneratedbycyclicelectronflowinChlamydomonasreinhardtii题目翻译：莱茵衣藻中通过环式电子传递产生的质子梯度控制光致产氢作者：摘要：阅读笔记：真核微藻的光致产氢，通过光合电子传递链和质体氢化酶之间的联系：“Hydrogenphotoproductionbyeukaryoticmicroalgaeresultsfromaconnectionbetweenthephotosynthetic

2、electrontransportchainandaplastidialhydrogenase.”藻类产氢，在自然条件下，通常是一种短暂的现象，通常被认为是一种避免光合电子传递链过度还原的一种保护安全阀：“AlgalH2productionisatransitoryphenomenonundermostnaturalconditions,oftenviewedasasafetyvalveprotectingthephotosyntheticelectrontransportchainfromoverreduction.”分析莱茵衣藻的突

3、变株，基于暗-光叶绿素荧光分析，分离出一株环绕PSI的环式电子传递CEF受损的突变株，由于其缺乏“质子梯度调节蛋白ProtonGradientRegulationLike1(PGRL1)protein”：“FromthecolonyscreeningofaninsertionmutantlibraryoftheunicellulargreenalgaChlamydomonasreinhardtiibasedontheanalysisofdark-lightchlorophyllfluorescencetransients,weisola

4、tedamutantimpairedincyclicelectronflowaroundphotosystemI(CEF)duetoadefectintheProtonGradientRegulationLike1(PGRL1)protein.”在好氧生活条件下，在突变株pgrl1中，非光化学淬灭（NPQ）显著降低：“Underaerobiosis,nonphotochemicalquenchingoffluorescence(NPQ)isstronglydecreasedinpgrl1.”在厌氧生活条件下，在突变株pgrl1中的光致产

5、氢显著增加，无论是在短期还是长期测量中（缺硫条件下）：“Underanaerobiosis,H2photoproductionisstronglyenhancedinthepgrl1mutant,bothduringshort-termandlong-termmeasurements(inconditionsofsulfurdeprivation).”根据NPQ和产生氢气的光依赖性，同时，在加入解耦联剂FCCP（uncouplingagentcarbonylcyanidep-trifluoromethoxyphenylhydrazone

6、(FCCP)）时野生型的产氢量也增加，得出结论：CEF产生的质子梯度引起野生型中氢化酶的电子供应抑制，而在突变株pgrl1中是没有这种抑制的：“BasedonthelightdependenceofNPQandhydrogenproduction,aswellasontheenhancedhydrogenproductionobservedinthewild-typestraininthepresenceoftheuncouplingagentcarbonylcyanidep-trifluoromethoxyphenylhydrazon

7、e,weconcludethattheprotongradientgeneratedbyCEFprovokesastronginhibitionofelectronsupplytothehydrogenaseinthewild-typestrain,whichisreleasedinthepgrl1mutant.”通过检测pgrl1的表达对跨类囊体膜质子梯度的调节，展示了重新设计微藻细胞的代谢来增加氢气生产量的新视野：“Regulationofthetrans-thylakoidalprotongradientbymonitoringp

8、grl1expressionopensnewperspectivestowardreprogrammingthecellularmetabolismofmicroalgaeforenhancedH2prod