McLean K M, Gutman P D, Minton K W, Clark E P
Armed Forces Radiobiology Research Institute, Bethesda, Maryland 20889-5145.
Radiat Res. 1992 Jun;130(3):366-71.
Cells cope with radiation damage through several mechanisms: (1) increased DNA repair activity, (2) scavenging and inactivation of radiation-induced radical molecules, and (3) entry into a G0-like quiescent state. We have investigated a chromosomal rearrangement to elucidate further the molecular and genetic mechanisms underlying these phenomena. A mutant of Escherichia coli JM83 (phi 80dlacZ delta M15) was isolated that demonstrated significantly increased resistance to both ionizing and ultraviolet radiation. Surviving fractions of mutant and wild-type cells were measured following exposure to standardized doses of radiation. Increased radioresistance was directly related to a chromosomal alteration near the bacteriophage phi 80 attachment site (attB), as initially detected by the LacZ- phenotype of the isolate. Southern hybridization of chromosomal DNA from the mutant and wild-type E. coli JM83 strains indicated that a deletion had occurred. We propose that the deletion near the attB locus produces the radioresistant phenotype of the E. coli JM83 LacZ- mutant, perhaps through the alteration or inactivation of a gene or its controlling element(s).
(1)增强DNA修复活性;(2)清除并使辐射诱导的自由基分子失活;(3)进入类似G0的静止状态。我们研究了一种染色体重排,以进一步阐明这些现象背后的分子和遗传机制。分离出了大肠杆菌JM83(phi 80dlacZ delta M15)的一个突变体,该突变体对电离辐射和紫外线辐射均表现出显著增强的抗性。在暴露于标准化辐射剂量后,测量了突变体和野生型细胞的存活分数。辐射抗性的增加与噬菌体phi 80附着位点(attB)附近的染色体改变直接相关,最初是通过分离株的LacZ-表型检测到的。来自突变型和野生型大肠杆菌JM83菌株的染色体DNA的Southern杂交表明发生了缺失。我们提出,attB位点附近的缺失产生了大肠杆菌JM83 LacZ-突变体的抗辐射表型,可能是通过一个基因或其控制元件的改变或失活。