Walker J R, Pardee A B
J Bacteriol. 1967 Jan;93(1):107-14. doi: 10.1128/jb.93.1.107-114.1967.
The lon(-) mutation is responsible for a defect in cell division of Escherichia coli lightly irradiated with ultraviolet light (UV). These lon(-) mutants can be isolated readily by a procedure described here. Physiological studies were performed with the objective of determining the role of the lon gene. Unirradiated lon(-) mutants grow normally, except that a correlation of this mutation with capsule formation has been noted previously. These two properties can be separated, however. After irradiation, lon(-) grows as long filaments because septum formation is prevented. The filaments eventually lyse. Mass increase and deoxyribonucleic acid and enzyme synthesis appear to proceed normally. Thus, the lesion produced by UV appears to be highly specific. In bacteria that carry both genes (merozygotes), lon(+) is dominant to lon(-). Septum formation is restored to irradiated lon(-) bacteria by introduction of lon(+) by conjugation. Also, normal growth can be restored by nutritional variations. It is concluded that lon(+) is able to nullify the effects of the UV lesion under conditions where lon(-) cannot. Possibly, capsule precursors that can accumulate in the latter are responsible for the difference because they interfere with repair of the UV lesion.
lon(-)突变导致轻度紫外线(UV)照射的大肠杆菌细胞分裂出现缺陷。通过本文所述的方法可以轻松分离出这些lon(-)突变体。进行生理学研究的目的是确定lon基因的作用。未照射的lon(-)突变体正常生长,只是此前已注意到这种突变与荚膜形成有关。然而,这两种特性是可以分开的。照射后,lon(-)会生长成很长的细丝,因为隔膜形成受到阻碍。这些细丝最终会裂解。质量增加以及脱氧核糖核酸和酶的合成似乎正常进行。因此,紫外线产生的损伤似乎具有高度特异性。在同时携带这两个基因的细菌(部分二倍体)中,lon(+)对lon(-)呈显性。通过接合引入lon(+)可使照射后的lon(-)细菌恢复隔膜形成。此外,营养变化也可恢复正常生长。得出的结论是,在lon(-)无法做到的条件下,lon(+)能够消除紫外线损伤的影响。可能是后者中积累的荚膜前体导致了这种差异,因为它们会干扰紫外线损伤的修复。