Prince R C, Daldal F
Exxon Research and Engineering, Annandale, NJ 08801.
Biochim Biophys Acta. 1987 Dec 17;894(3):370-8. doi: 10.1016/0005-2728(87)90115-0.
The nature and number of physiological electron donors to the photochemical reaction center of Rhodobacter capsulatus have been probed by deleting the genes for cytochromes c1 and b of the cytochrome bc1 complex, alone or in combination with deletion of the gene for cytochrome c2. Deletion of cytochrome c1 renders the organism incapable of photosynthetic growth, regardless of the presence or absence of cytochrome c2, because in the absence of the bc1 complex there is no cyclic electron transfer, nor any alternative source of electrons to rereduce the photochemically oxidized reaction center. While cytochrome c2 is capable of reducing the reaction center, there appears no alternative route for its rereduction other than the bc1 complex. The deletion of cytochromes c1 and c2 reveals previously unrecognized membrane-bound and soluble high potential c-type cytochromes, with Em7 = +312 mV and Em6.5 = +316 mV, respectively. These cytochromes do not donate electrons to the reaction center, and their roles are unknown.
通过单独缺失细胞色素bc1复合物的细胞色素c1和b基因,或与细胞色素c2基因缺失相结合,研究了荚膜红细菌光化学反应中心的生理电子供体的性质和数量。无论细胞色素c2是否存在,细胞色素c1的缺失都会使该生物体无法进行光合生长,因为在没有bc1复合物的情况下,不存在循环电子传递,也没有任何替代电子源来重新还原光化学氧化的反应中心。虽然细胞色素c2能够还原反应中心,但除了bc1复合物外,似乎没有其他途径对其进行重新还原。细胞色素c1和c2的缺失揭示了以前未被认识的膜结合型和可溶性高电位c型细胞色素,其Em7分别为+312 mV和Em6.5为+316 mV。这些细胞色素不会向反应中心提供电子,它们的作用尚不清楚。