Zdzienicka M Z, Mitchell D L, Venema J, van Hoffen A, van Zeeland A A, Mullenders L H, de Wit J, Simons J W
MGC-Department of Radiation Genetics and Chemical Mutagenesis, State University of Leiden, Sylvius Laboratory, The Netherlands.
Mutagenesis. 1991 May;6(3):179-83. doi: 10.1093/mutage/6.3.179.
The V79 Chinese hamster cell mutant V-B11 has previously been assigned to a new complementation group (group 7) of UV-sensitive rodent mutants. The D10 for cell survival is approximately 6 J/m2 for V-B11, compared with approximately 15 J/m2 for the parental V79 cell line. The removal of (6-4) photoproducts from the genome overall is not impaired in V-B11, and the level of unscheduled DNA synthesis measured 2 h after UV irradiation is similar to that observed in the parental V79 cells. DNA repair replication measured as a function of UV dose is approximately 50% reduced in V-B11 in comparison with V79, when measured during the first 6 h after UV irradiation. Furthermore, in V-B11 the rate of cyclobutane dimer removal from the HPRT gene is slower than in wild-type cells. Despite the observed defects no effect on the UV-induced frequency of mutants at two loci: Na+/K(+)-ATPase and HPRT was found in V-B11 cells. The properties of V-B11 are compared with those of other UV-sensitive mutants.
V79中国仓鼠细胞突变体V - B11先前已被归入对紫外线敏感的啮齿动物突变体的一个新的互补群(第7组)。V - B11细胞存活的D10约为6 J/m²,而亲本V79细胞系约为15 J/m²。V - B11中从基因组整体去除(6 - 4)光产物的过程未受损害,紫外线照射2小时后测得的非预定DNA合成水平与亲本V79细胞中观察到的相似。与V79相比,在紫外线照射后的最初6小时内测量时,V - B11中作为紫外线剂量函数的DNA修复复制减少了约50%。此外,在V - B11中,从HPRT基因去除环丁烷二聚体的速率比野生型细胞慢。尽管观察到这些缺陷,但在V - B11细胞中未发现对两个位点(Na⁺/K⁺ - ATP酶和HPRT)紫外线诱导的突变频率有影响。将V - B11的特性与其他对紫外线敏感的突变体的特性进行了比较。