Leong J, Neilands J B
J Bacteriol. 1976 May;126(2):823-30. doi: 10.1128/jb.126.2.823-830.1976.
Uptake of 55Fe- and 3H-labeled siderophores and their chronic analogues have been studied in Salmonella typhimurium LT-2 and Escherichia coli K-12. In S. typhimurium LT-2, at least two different mechanisms for siderophore iron transport may be operative. Uptake of 55Fe- and 3H-labeled ferrichrome and kinetically inert lambda-cis-chromic [3H]deferriferrichrome by the S. typhimurium LT-2 enb7 mutant, which is defective in the production of its native siderophore, enterobactin, appears to occur by two concurrent mechanisms. The first mechanism is postulated to involve either rapid uptake of iron released from the ferric complex by cellular reduction without penetration of the complex or ligand or dissociation of the complex and simultaneous uptake of both ligand and iron coupled with simultaneous expulsion of the ligand. The second mechanism appears to consist of slower uptake of the intact ferric complex.
已在鼠伤寒沙门氏菌LT-2和大肠杆菌K-12中研究了55Fe和3H标记的铁载体及其慢性类似物的摄取情况。在鼠伤寒沙门氏菌LT-2中,铁载体铁转运至少可能有两种不同机制起作用。鼠伤寒沙门氏菌LT-2 enb7突变体自身的铁载体肠杆菌素产生存在缺陷,该突变体对55Fe和3H标记的高铁色素以及动力学惰性的λ-顺式-铬[3H]去铁高铁色素的摄取似乎通过两种并行机制发生。第一种机制假定涉及通过细胞还原从铁复合物中释放的铁的快速摄取,而复合物、配体不穿透或复合物解离,同时摄取配体和铁,并同时排出配体。第二种机制似乎包括完整铁复合物的较慢摄取。