Theis James F, Dershowitz Ann, Irene Carmela, Maciariello Clelia, Tobin Michael L, Liberi Giordano, Tabrizifard Sahba, Korus Malgorzata, Fabiani Lucia, Newlon Carol S
Department of Microbiology and Molecular Genetics, UMDNJ-New Jersey Medical School, Newark, New Jersey 07103, USA.
Genetics. 2007 Nov;177(3):1445-58. doi: 10.1534/genetics.107.074690. Epub 2007 Aug 24.
Eukaryotic chromosomes are duplicated during S phase and transmitted to progeny during mitosis with high fidelity. Chromosome duplication is controlled at the level of replication initiation, which occurs at cis-acting replicator sequences that are spaced at intervals of approximately 40 kb along the chromosomes of the budding yeast Saccharomyces cerevisiae. Surprisingly, we found that derivatives of yeast chromosome III that lack known replicators were replicated and segregated properly in at least 96% of cell divisions. To gain insight into the mechanisms that maintain these "originless" chromosome fragments, we screened for mutants defective in the maintenance of an "originless" chromosome fragment, but proficient in the maintenance of the same fragment that carries its normal complement of replicators (originless fragment maintenance mutants, or ofm). We show that three of these Ofm mutations appear to disrupt different processes involved in chromosome transmission. The OFM1-1 mutant seems to disrupt an alternative initiation mechanism, and the ofm6 mutant appears to be defective in replication fork progression. ofm14 is an allele of RAD9, which is required for the activation of the DNA damage checkpoint, suggesting that this checkpoint plays a key role in the maintenance of the "originless" fragment.
真核生物染色体在S期进行复制,并在有丝分裂期间以高保真度传递给子代。染色体复制在复制起始水平受到控制,复制起始发生在顺式作用复制子序列上,这些序列沿着芽殖酵母酿酒酵母的染色体以大约40 kb的间隔分布。令人惊讶的是,我们发现缺少已知复制子的酵母III号染色体衍生物在至少96%的细胞分裂中能够正常复制和分离。为了深入了解维持这些“无起始点”染色体片段的机制,我们筛选了在维持“无起始点”染色体片段方面有缺陷,但在维持携带其正常复制子互补序列的相同片段方面 proficient(此处原文可能有误,推测为“ proficient”,意为熟练的、精通的,暂按此翻译为“ proficient”)的突变体(无起始点片段维持突变体,或ofm)。我们表明,这些Ofm突变中的三个似乎破坏了参与染色体传递的不同过程。OFM1 - 1突变体似乎破坏了一种替代起始机制,而ofm6突变体在复制叉进展方面似乎存在缺陷。ofm14是RAD9的一个等位基因,DNA损伤检查点的激活需要RAD9,这表明该检查点在维持“无起始点”片段中起关键作用。