Huokko Tuomas, Muth-Pawlak Dorota, Battchikova Natalia, Allahverdiyeva Yagut, Aro Eva-Mari
Laboratory of Molecular Plant Biology, Department of Biochemistry, University of Turku, Turku FI-20014, Finland.
Laboratory of Molecular Plant Biology, Department of Biochemistry, University of Turku, Turku FI-20014, Finland
Plant Physiol. 2017 Jul;174(3):1863-1880. doi: 10.1104/pp.17.00398. Epub 2017 May 22.
NAD(P)H dehydrogenases comprise type 1 (NDH-1) and type 2 (NDH-2s) enzymes. Even though the NDH-1 complex is a well-characterized protein complex in the thylakoid membrane of sp. PCC 6803 (hereafter ), the exact roles of different NDH-2s remain poorly understood. To elucidate this question, we studied the function of NdbC, one of the three NDH-2s in , by constructing a deletion mutant (Δ) for a corresponding protein and submitting the mutant to physiological and biochemical characterization as well as to comprehensive proteomics analysis. We demonstrate that the deletion of NdbC, localized to the plasma membrane, affects several metabolic pathways in in autotrophic growth conditions without prominent effects on photosynthesis. Foremost, the deletion of NdbC leads, directly or indirectly, to compromised sugar catabolism, to glycogen accumulation, and to distorted cell division. Deficiencies in several sugar catabolic routes were supported by severe retardation of growth of the Δ mutant under light-activated heterotrophic growth conditions but not under mixotrophy. Thus, NdbC has a significant function in regulating carbon allocation between storage and the biosynthesis pathways. In addition, the deletion of NdbC increases the amount of cyclic electron transfer, possibly via the NDH-1 complex, and decreases the expression of several transporters in ambient CO growth conditions.
NAD(P)H脱氢酶包括1型(NDH-1)和2型(NDH-2s)酶。尽管NDH-1复合物是聚球藻PCC 6803(以下简称)类囊体膜中一种特征明确的蛋白质复合物,但不同NDH-2s的确切作用仍知之甚少。为了阐明这个问题,我们通过构建相应蛋白质的缺失突变体(Δ)并对该突变体进行生理生化特性分析以及全面的蛋白质组学分析,研究了聚球藻中三种NDH-2s之一的NdbC的功能。我们证明,定位于质膜的NdbC的缺失在自养生长条件下影响聚球藻的几种代谢途径,而对光合作用没有显著影响。首先,NdbC的缺失直接或间接地导致糖分解代谢受损、糖原积累以及细胞分裂异常。在光激活的异养生长条件下但在混合营养条件下未出现这种情况,Δ突变体生长严重迟缓,这支持了几种糖分解途径存在缺陷。因此,NdbC在调节储存和生物合成途径之间的碳分配方面具有重要功能。此外,NdbC的缺失可能通过NDH-1复合物增加循环电子传递的量,并降低在环境CO生长条件下几种转运蛋白的表达。