铁氧还蛋白
塑料醌
电子传输链
渠化
叶绿体
类囊体
铁氧还蛋白NADP(+)还原酶
光合作用
生物物理学
硝酸还原酶
突变体
生物化学
亚硝酸盐还原酶
生物
化学
酶
有机化学
离子
基因
作者
Guy T. Hanke,Tsuyoshi Endo,Fumihiko Satoh,Toshiharu Hase
标识
DOI:10.1111/j.1365-3040.2008.01814.x
摘要
ABSTRACT The mechanism by which plants regulate channelling of photosynthetically derived electrons into different areas of chloroplast metabolism remains obscure. Possible fates of such electrons include use in carbon assimilation, nitrogen assimilation and redox signalling pathways, or return to the plastoquinone pool through cyclic electron flow. In higher plants, these electrons are made accessible to stromal enzymes, or for cyclic electron flow, as reduced ferredoxin (Fd), or NADPH. We investigated how knockout of an Arabidopsis ( Arabidopsis thaliana ) ferredoxin:NADPH reductase (FNR) isoprotein and the loss of strong thylakoid binding by the remaining FNR in this mutant affected the channelling of photosynthetic electrons into NADPH‐ and Fd‐dependent metabolism. Chlorophyll fluorescence data show that these mutants have complex variation in cyclic electron flow, dependent on light conditions. Measurements of electron transport in isolated thylakoid and chloroplast systems demonstrated perturbed channelling to NADPH‐dependent carbon and Fd‐dependent nitrogen assimilating metabolism, with greater competition in the mutant. Moreover, mutants accumulate greater biomass than the wild type under low nitrate growth conditions, indicating that such altered chloroplast electron channelling has profound physiological effects. Taken together, our results demonstrate the integral role played by FNR isoform and location in the partitioning of photosynthetic reducing power.
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