Nagarajan Sowmya, Srivastava Sanvesh, Sherman Louis A
Department of Biological Sciences, Purdue University, West Lafayette, IN, 47907, USA.
Mol Microbiol. 2014 Jan;91(1):79-97. doi: 10.1111/mmi.12442. Epub 2013 Nov 15.
The plasmid hik31 operon (P3, slr6039-slr6041) is located on the pSYSX plasmid in Synechocystis sp. PCC 6803. A P3 mutant (ΔP3) had a growth defect in the dark and a pigment defect that was worsened by the addition of glucose. The glucose defect was from incomplete metabolism of the substrate, was pH dependent, and completely overcome by the addition of bicarbonate. Addition of organic carbon and nitrogen sources partly alleviated the defects of the mutant in the dark. Electron micrographs of the mutant revealed larger cells with division defects, glycogen limitation, lack of carboxysomes, deteriorated thylakoids and accumulation of polyhydroxybutyrate and cyanophycin. A microarray experiment over two days of growth in light-dark plus glucose revealed downregulation of several photosynthesis, amino acid biosynthesis, energy metabolism genes; and an upregulation of cell envelope and transport and binding genes in the mutant. ΔP3 had an imbalance in carbon and nitrogen levels and many sugar catabolic and cell division genes were negatively affected after the first dark period. The mutant suffered from oxidative and osmotic stress, macronutrient limitation, and an energy deficit. Therefore, the P3 operon is an important regulator of central metabolism and cell division in the dark.
质粒hik31操纵子（P3，slr6039 - slr6041）位于集胞藻PCC 6803的pSYSX质粒上。P3突变体（ΔP3）在黑暗中存在生长缺陷以及色素缺陷，添加葡萄糖会使色素缺陷加剧。葡萄糖缺陷源于底物的不完全代谢，与pH有关，添加碳酸氢盐可完全克服该缺陷。添加有机碳源和氮源可部分缓解突变体在黑暗中的缺陷。突变体的电子显微镜照片显示细胞更大且存在分裂缺陷、糖原受限、缺乏羧酶体、类囊体退化以及聚羟基丁酸酯和蓝藻素积累。一项在明暗交替加葡萄糖条件下进行两天生长的微阵列实验表明，突变体中几个光合作用、氨基酸生物合成、能量代谢基因下调；而细胞包膜、转运和结合基因上调。ΔP3在碳和氮水平上存在失衡，在第一个黑暗期后许多糖分解代谢和细胞分裂基因受到负面影响。该突变体遭受氧化和渗透胁迫、大量营养物质限制以及能量不足。因此，P3操纵子是黑暗中中心代谢和细胞分裂的重要调节因子。
