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首页> 外文期刊>Molecular and Cellular Biology >Specific DNA replication mutations affect telomere length in Saccharomyces cerevisiae.
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Specific DNA replication mutations affect telomere length in Saccharomyces cerevisiae.

机译：特定的DNA复制突变会影响酿酒酵母中的端粒长度。

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To investigate the relationship between the DNA replication apparatus and the control of telomere length, we examined the effects of several DNA replication mutations on telomere length in Saccharomyces cerevisiae. We report that a mutation in the structural gene for the large subunit of DNA replication factor C (cdc44/rfc1) causes striking increases in telomere length. A similar effect is seen with mutations in only one other DNA replication gene: the structural gene for DNA polymerase alpha (cdc17/pol1) (M.J. Carson and L. Hartwell, Cell 42:249-257, 1985). For both genes, the telomere elongation phenotype is allele specific and appears to correlate with the penetrance of the mutations. Furthermore, fluorescence-activated cell sorter analysis reveals that those alleles that cause elongation also exhibit a slowing of DNA replication. To determine whether elongation is mediated by telomerase or by slippage of the DNA polymerase, we created cdc17-1 mutants carrying deletions of the gene encoding the RNA component of telomerase (TLC1). cdc17-1 strains that would normally undergo telomere elongation failed to do so in the absence of telomerase activity. This result implies that telomere elongation in cdc17-1 mutants is mediated by the action of telomerase. Since DNA replication involves transfer of the nascent strand from polymerase alpha to replication factor C (T. Tsurimoto and B. Stillman, J. Biol. Chem. 266:1950-1960, 1991; T. Tsurimoto and B. Stillman, J. Biol. Chem. 266:1961-1968, 1991; S. Waga and B. Stillman, Nature [London] 369:207-212, 1994), one possibility is that this step affects the regulation of telomere length.
机译：为了研究DNA复制装置和端粒长度控制之间的关系，我们检查了酿酒酵母中几个DNA复制突变对端粒长度的影响。我们报告说，DNA复制因子C（cdc44 / rfc1）的大亚基的结构基因中的突变导致端粒长度显着增加。仅在另一个DNA复制基因中的突变上可以看到类似的效果：DNA聚合酶α的结构基因（cdc17 / pol1）（M.J.Carson和L.Hartwell，Cell 42：249-257，1985）。对于这两个基因，端粒延长表型是等位基因特异性的，并且似乎与突变的渗透率相关。此外，荧光激活的细胞分选仪分析表明，那些引起伸长的等位基因也表现出DNA复制的减慢。为了确定延长是由端粒酶介导还是由DNA聚合酶的滑动介导，我们创建了cdc17-1突变体，该突变体携带编码端粒酶（TLC1）RNA成分的基因的缺失。在缺乏端粒酶活性的情况下，通常会进行端粒延长的cdc17-1菌株无法这样做。该结果暗示cdc17-1突变体中的端粒延长是由端粒酶的作用介导的。由于DNA复制涉及将新生链从聚合酶α转移到复制因子C（T. Tsurimoto和B.Stillman，J.Biol.Chem.266：1950-1960，1991; T.Tsurimoto和B.Stillman，J.Biol Chem.266：1961-1968，1991; S.Waga和B.Stillman，Nature [London] 369：207-212，1994），一种可能性是该步骤影响端粒长度的调节。

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