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Mapping the Polarity of Changes That Occur in Interrupted CAG Repeat Tracts in Yeast

机译：映射酵母中CAG重复序列中断发生的变化的极性

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To explore the mechanisms by which CAG trinucleotide repeat tracts undergo length changes in yeast cells, we examined the polarity of alterations with respect to an interrupting CAT trinucleotide near the center of the tract. In wild-type cells, in which most tract changes are large contractions, the changes that retain the interruption are biased toward the 3′ end of the repeat tract (in reference to the direction of lagging-strand synthesis). In rth1/rad27mutant cells that are defective in Okazaki fragment maturation, the tract expansions are biased to the 5′ end of the repeat tract, while the tract contractions that do not remove the interruption occur randomly on either side of the interruption. In msh2 mutant cells that are defective in the mismatch repair machinery, neither the small changes of one or two repeat units nor the larger contractions attributable to this mutation are biased to either side of the interruption. The results of this study are discussed in terms of the molecular paths leading to expansions and contractions of repeat tracts.
机译：为了探索CAG三核苷酸重复序列在酵母细胞中发生长度变化的机制，我们检查了在该通道中央附近的CAT三核苷酸中断的改变极性。在大多数道变化为大收缩的野生型细胞中，保留中断的变化偏向重复道的3'端（参考滞后链合成的方向）。在冈崎片段成熟缺陷的 rth1 / rad27 突变细胞中，束扩展偏向重复束的5'端，而不能消除中断的束收缩随机发生在任一中断的一面。在错配修复机制中有缺陷的 msh2 突变细胞中，一个或两个重复单元的微小变化或归因于该突变的较大收缩都不会偏向中断的任一侧。本研究的结果讨论了导致重复序列膨胀和收缩的分子途径。

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