Takagaki Y, Matsuhashi M, Yamashita J, Horio T
J Bacteriol. 1977 Jul;131(1):229-39. doi: 10.1128/jb.131.1.229-239.1977.
Colicin K greatly decreased the incorporation of 32P-labeled inorganic orthophosphate into nucleotides and nucleic acids, causing a concomitant increase in the formation of 32P-labeled sugar phosphates in sensitive cells of Escherichia coli. These sugar phosphates were formed in aerobically growing cells, as well as in cells under stringent control of ribonucleic acid synthesis. The main 32P-labeled product was identified as sedoheptulose 7-phosphate in two strains (B1 and K-12 MK-1) and fructose 1,6-diphosphate in one strain (K-12 CP78). The formation of sugar phosphates induced by colicin K was inhibited by carbonyl cyanide m-chlorophenylhydrazone. It was also not observed in N,N'-dicyclohexylcarbodiimide-treated cells or Mg2+-(Ca2+)-adenosine triphosphatase-less mutant (strain K-12 AN120) cells. Thus, the formation of sugar phosphates in colicin K-treated cells is dependent on the formation of adenosine 5'-triphosphate by oxidative phosphorylation.
大肠菌素K显著降低了32P标记的无机正磷酸盐掺入核苷酸和核酸中的量,导致大肠杆菌敏感细胞中32P标记的磷酸糖形成量相应增加。这些磷酸糖在需氧生长的细胞以及处于核糖核酸合成严格控制下的细胞中形成。在两个菌株(B1和K - 12 MK - 1)中,主要的32P标记产物被鉴定为景天庚酮糖7 - 磷酸,在一个菌株(K - 12 CP78)中为果糖1,6 - 二磷酸。羰基氰化物间氯苯腙抑制了大肠菌素K诱导的磷酸糖形成。在N,N'-二环己基碳二亚胺处理的细胞或Mg2 + -(Ca2 +)-腺苷三磷酸酶缺陷型突变体(菌株K - 12 AN120)细胞中也未观察到这种现象。因此,大肠菌素K处理的细胞中磷酸糖的形成依赖于通过氧化磷酸化形成腺苷5'-三磷酸。