Fleer R, Nicolet C M, Pure G A, Friedberg E C
Mol Cell Biol. 1987 Mar;7(3):1180-92. doi: 10.1128/mcb.7.3.1180-1192.1987.
In contrast to other Saccharomyces cerevisiae RAD genes involved in nucleotide excision repair of DNA, the RAD4 gene could not be isolated by screening a yeast genomic library for recombinant plasmids which complement the UV sensitivity of rad4 mutants (Pure et al., J. Mol. Biol. 183:31-42, 1985). We therefore attempted to walk to RAD4 from the neighboring SPT2 gene and obtained an integrating derivative of a plasmid isolated by Roeder et al. (Mol. Cell. Biol. 5:1543-1553, 1985) which contains a 4-kilobase fragment of yeast DNA including a mutant allele of SPT2. When integrated into several different rad4 mutant strains, this plasmid (pR169) complements UV sensitivity at a frequency of approximately 10%. However, a centromeric plasmid containing rescued sequences which include flanking yeast DNA no longer complements the phenotype of rad4 mutants. Complementing activity was restored by in vivo repair of a defined gap in the centromeric plasmid. The repaired plasmid fully complements the UV sensitivity of all rad4 mutants tested when isolated directly from yeast cells, but when this plasmid is propagated in Escherichia coli complementing activity is lost. We have mapped the physical location of the RAD4 gene by insertional mutagenesis and by transcript mapping. The gene is approximately 2.3 kilobases in size and is located immediately upstream of the SPT2 gene. Both genes are transcribed in the same direction. RAD4 is not an essential gene, and no increased transcription of this gene is observed in cells exposed to the DNA-damaging agent 4-nitroquinoline-1-oxide. The site of inactivation of RAD4 in a particular plasmid propagated in E. coli was localized to a 100-base-pair region by gene disruption and gap repair experiments. In addition, we have identified the approximate locations of the chromosomal rad4-2, rad4-3, and rad4-4 mutations.
与参与DNA核苷酸切除修复的其他酿酒酵母RAD基因不同,通过筛选酵母基因组文库以寻找能互补rad4突变体紫外线敏感性的重组质粒,无法分离出RAD4基因(Pure等人,《分子生物学杂志》183:31 - 42,1985年)。因此,我们试图从相邻的SPT2基因向RAD4进行染色体步移,并获得了Roeder等人(《分子与细胞生物学》5:1543 - 1553,1985年)分离的一个质粒的整合衍生物,该质粒包含一段4千碱基的酵母DNA片段,其中包括SPT2的一个突变等位基因。当整合到几种不同的rad4突变菌株中时,该质粒(pR169)以约10%的频率互补紫外线敏感性。然而,一个含有拯救序列(包括侧翼酵母DNA)的着丝粒质粒不再能互补rad4突变体的表型。通过在体内修复着丝粒质粒中的一个特定缺口,恢复了互补活性。直接从酵母细胞中分离时,修复后的质粒能完全互补所有测试的rad4突变体的紫外线敏感性,但当该质粒在大肠杆菌中繁殖时,互补活性丧失。我们通过插入诱变和转录图谱分析确定了RAD4基因的物理位置。该基因大小约为2.3千碱基,位于SPT2基因的紧邻上游。两个基因转录方向相同。RAD4不是必需基因,在暴露于DNA损伤剂4 - 硝基喹啉 - 1 - 氧化物的细胞中未观察到该基因转录增加。通过基因破坏和缺口修复实验,将在大肠杆菌中繁殖的一个特定质粒中RAD4的失活位点定位到一个100碱基对的区域。此外,我们还确定了染色体上rad4 - 2、rad4 - 3和rad4 - 4突变的大致位置。