Iuchi S, Cole S T, Lin E C
Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115.
J Bacteriol. 1990 Jan;172(1):179-84. doi: 10.1128/jb.172.1.179-184.1990.
In Escherichia coli, sn-glycerol-3-phosphate can be oxidized by two different flavo-dehydrogenases, an anaerobic enzyme encoded by the glpACB operon and an aerobic enzyme encoded by the glpD operon. These two operons belong to the glp regulon specifying the utilization of glycerol, sn-glycerol-3-phosphate, and glycerophosphodiesters. In glpR mutant cells grown under conditions of low catabolite repression, the glpA operon is best expressed anaerobically with fumarate as the exogenous electron acceptor, whereas the glpD operon is best expressed aerobically. Increased anaerobic expression of glpA is dependent on the fnr product, a pleiotropic activator of genes involved in anaerobic respiration. In this study we found that the expression of a glpA1(Oxr) (oxygen-resistant) mutant operon, selected for increased aerobic expression, became less dependent on the FNR protein but more dependent on the cyclic AMP-catabolite gene activator protein complex mediating catabolite repression. Despite the increased aerobic expression of glpA1(Oxr), a twofold aerobic repressibility persisted. Moreover, anaerobic repression by nitrate respiration remained normal. Thus, there seems to exist a redox control apart from the FNR-mediated one. We also showed that the anaerobic repression of the glpD operon was fully relieved by mutations in either arcA (encoding a presumptive DNA recognition protein) or arcB (encoding a presumptive redox sensor protein). The arc system is known to mediate pleiotropic control of genes of aerobic function.
在大肠杆菌中,sn-甘油-3-磷酸可被两种不同的黄素脱氢酶氧化,一种是由glpACB操纵子编码的厌氧酶,另一种是由glpD操纵子编码的需氧酶。这两个操纵子属于glp调节子,该调节子决定甘油、sn-甘油-3-磷酸和甘油磷酸二酯的利用。在低分解代谢物阻遏条件下生长的glpR突变细胞中,glpA操纵子在以富马酸作为外源电子受体时厌氧条件下表达最佳,而glpD操纵子在需氧条件下表达最佳。glpA厌氧表达的增加依赖于fnr产物,它是参与厌氧呼吸的基因的多效性激活剂。在本研究中,我们发现为增加需氧表达而选择的glpA1(Oxr)(耐氧)突变操纵子的表达变得对FNR蛋白的依赖性降低,但对介导分解代谢物阻遏的环腺苷酸-分解代谢物基因激活蛋白复合物的依赖性增加。尽管glpA1(Oxr)的需氧表达增加,但仍存在两倍的需氧可阻遏性。此外,硝酸盐呼吸的厌氧阻遏保持正常。因此,似乎除了FNR介导的氧化还原控制之外还存在另一种氧化还原控制。我们还表明,arcA(编码一种假定的DNA识别蛋白)或arcB(编码一种假定的氧化还原传感器蛋白)中的突变可完全解除glpD操纵子的厌氧阻遏。已知arc系统介导对有氧功能基因的多效性控制。