Herschman H R, Helinski D R
J Bacteriol. 1967 Sep;94(3):691-9. doi: 10.1128/jb.94.3.691-699.1967.
Colicinogenic factors ColI and ColV, which have been shown to behave as sex factors, could not be induced with mitomycin C. In contrast, the ColE(1), ColE(2), and ColE(3) factors, which do not exhibit any fertility factor characteristics, are inducible by this agent. The induced production of colicins E(1), E(2), and E(3) was accompanied by a loss in viability at a concentration of mitomycin C which was bacteriostatic to noncolicinogenic cells or to cells carrying the ColV or ColI factors. The loss in viability accompanying the mitomycin C induction of the ColE(1), ColE(2), or ColE(3) factors also occurred when colicin synthesis was blocked by chloramphenicol or amino acid starvation. However, chloramphenicol was able to block the loss of viability of a recipient cell after mitomycin C induction of a newly acquired Col factor if the antibiotic was present throughout the mating period. No detectable internal colicin or colicin precursor could be demonstrated during the lag period prior to the appearance of colicin outside the cell 20 to 30 min after the addition of mitomycin C. If chloramphenicol was present during the lag period following the addition of mitomycin C, colicin synthesis began immediately after the removal of these antibiotics. The synthesis of tryptophan synthetase and induced beta-galactosidase proceeded normally throughout the lag period and well into the period of colicin production. Regulation of beta-galactosidase synthesis did not seem to be profoundly affected during the lag period subsequent to mitomycin C addition. Induced colicin synthesis, like bacterial or induced prophage protein synthesis, was subject to inhibition by virulent phage infection.
产大肠杆菌素因子ColI和ColV已被证明具有性因子的行为,不能被丝裂霉素C诱导。相比之下,不表现出任何育性因子特征的ColE(1)、ColE(2)和ColE(3)因子可被该试剂诱导。在对非产大肠杆菌素细胞或携带ColV或ColI因子的细胞具有抑菌作用的丝裂霉素C浓度下,诱导产生大肠杆菌素E(1)、E(2)和E(3)伴随着活力丧失。当大肠杆菌素合成被氯霉素或氨基酸饥饿阻断时,丝裂霉素C诱导ColE(1)、ColE(2)或ColE(3)因子也会出现活力丧失。然而,如果在整个交配期都存在抗生素,氯霉素能够阻止丝裂霉素C诱导新获得的Col因子后受体细胞的活力丧失。在添加丝裂霉素C后20至30分钟细胞外出现大肠杆菌素之前的延迟期内,未检测到可检测到的细胞内大肠杆菌素或大肠杆菌素前体。如果在添加丝裂霉素C后的延迟期内存在氯霉素,在去除这些抗生素后大肠杆菌素合成立即开始。色氨酸合成酶和诱导型β-半乳糖苷酶的合成在整个延迟期以及大肠杆菌素产生期都正常进行。在添加丝裂霉素C后的延迟期内,β-半乳糖苷酶合成的调节似乎没有受到深刻影响。诱导的大肠杆菌素合成,如细菌或诱导的原噬菌体蛋白质合成,受到烈性噬菌体感染的抑制。