Watanabe H, Hashimoto H, Mitsuhashi S
J Bacteriol. 1980 Apr;142(1):145-52. doi: 10.1128/jb.142.1.145-152.1980.
Plasmid Rms312, specifying resistance to tetracycline (Tc), chloramphenicol (Cm), streptomycin (Sm), sulfonamide (Su), and mercury chloride (Mer), deletes both Tc and Cm Sm Su Mer determinants at a high frequency in Salmonella typhimurium LT2. S. typhimurium mutants that were stable carriers of Rms312 were isolated by alternate culture of R-bearing cells in a medium containing either tetracycline or chloramphenicol. In one of these mutants the deletion frequency of drug resistance determinants was decreased by about 100-fold not only Rms312, but also in R100, R1, and R6-5. This mutation caused a slight reduction of ultraviolet resistance but did not affect generalized genetic recombination, indicating that the mutation is different from recA. The mutation, designated dor (deletion of r-determinants), was mapped to a position near 57 units in the new linkage map of S. typhimurijm LT2 (K. E. Sanderson and P. E. Hartman, Microbiol. Rev. 42:471-519, 1978). The dor mutation had no effect on IS1-mediated illegitimate deletion, indicating that the dor mutation is different from the del mutation described by Nevers and Saedler (P. Nevers and H. Saedler, Mol. Gen. Genet. 160:209-214, 1978).
质粒Rms312赋予对四环素(Tc)、氯霉素(Cm)、链霉素(Sm)、磺胺(Su)和氯化汞(Mer)的抗性,它在鼠伤寒沙门氏菌LT2中能高频删除Tc、Cm、Sm、Su和Mer决定簇。通过在含有四环素或氯霉素的培养基中交替培养携带Rms312的细胞,分离出了稳定携带Rms312的鼠伤寒沙门氏菌突变体。在其中一个突变体中,不仅Rms312的耐药决定簇删除频率降低了约100倍,R100、R1和R6 - 5的耐药决定簇删除频率也降低了。这种突变导致紫外线抗性略有降低,但不影响广义遗传重组,这表明该突变不同于recA。该突变被命名为dor(r - 决定簇缺失),在鼠伤寒沙门氏菌LT2的新连锁图谱中被定位到靠近57个单位的位置(K. E. 桑德森和P. E. 哈特曼,《微生物学评论》42:471 - 519,1978)。dor突变对IS1介导的非法删除没有影响,这表明dor突变不同于内弗斯和赛德勒描述的del突变(P. 内弗斯和H. 赛德勒,《分子遗传学与普通遗传学》160:209 - 214,1978)。