Templin A, Kushner S R, Clark A J
Genetics. 1972 Oct;72(2):105-15.
Mutations in sbcB inactivate exonuclease I and suppress the UV-sensitive, mitomycin-sensitive, recombination-deficient phenotypes associated with recB and recC mutations. Mapping experiments have located sbcB about 0.4 minutes from the his operon at 38.0 on the standard map of E. coli. This places sbcB between supD and his. A four-point cross shows that sbcB lies between P2 attH and his. P2 eduction deleting the his operon beginning with P2 attH also deletes sbcB and produces the expected exonuclease I deficiency and suppression of recB(-). The occurrence of chemical-mutagen-induced and spontaneous mutations indirectly suppressing recB(-) and recC(-) is examined. Three lines of strains produce only sbcA mutations while only sbcB mutations occur in a fourth line. Explanations for this behavior are proposed in light of the ability of the first three lines to express sbcB mutations which they inherit by transduction.
sbcB 基因的突变会使核酸外切酶 I 失活，并抑制与 recB 和 recC 突变相关的紫外线敏感、丝裂霉素敏感、重组缺陷表型。定位实验已将 sbcB 定位在大肠杆菌标准图谱上 38.0 处，距离 his 操纵子约 0.4 分钟。这使得 sbcB 位于 supD 和 his 之间。四点杂交表明 sbcB 位于 P2 attH 和 his 之间。从 P2 attH 开始删除 his 操纵子的 P2 诱导也会删除 sbcB，并产生预期的核酸外切酶 I 缺陷和 recB(-) 的抑制。研究了化学诱变剂诱导的和自发的间接抑制 recB(-) 和 recC(-) 的突变的发生情况。三株菌株只产生 sbcA 突变，而第四株只出现 sbcB 突变。根据前三株菌株表达通过转导继承的 sbcB 突变的能力，对这种行为提出了解释。
