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首页> 外文期刊>Molecular and Cellular Biology >Intrachromatid Excision of Telomeric DNA as a Mechanism for Telomere Size Control in Saccharomyces cerevisiae
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Intrachromatid Excision of Telomeric DNA as a Mechanism for Telomere Size Control in Saccharomyces cerevisiae

机译：端粒DNA的染色体内切除作为酿酒酵母端粒大小控制的机制。

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We have previously identified a process in the yeastSaccharomyces cerevisiae that results in the contraction of elongated telomeres to wild-type length within a few generations. We have termed this process telomeric rapid deletion (TRD). In this study, we use a combination of physical and genetic assays to investigate the mechanism of TRD. First, to distinguish among several recombinational and nucleolytic pathways, we developed a novel physical assay in which HaeIII restriction sites are positioned within the telomeric tract. Specific telomeres were subsequently tested for HaeIII site movement between telomeres and for HaeIII site retention during TRD. Second, genetic analyses have demonstrated that mutations inRAD50 and MRE11 inhibit TRD. TRD, however, is independent of the Rap1p C-terminal domain, a central regulator of telomere size control. Our results provide evidence that TRD is an intrachromatid deletion process in which sequences near the extreme terminus invade end-distal sequences and excise the intervening sequences. We propose that the Mre11p-Rad50p-Xrs2p complex prepares the invading telomeric overhang for strand invasion, possibly through end processing or through alterations in chromatin structure.
机译：先前我们已经在酵母中发现了一个过程，该过程在数代内导致伸长的端粒收缩至野生型长度。我们称此过程为端粒快速缺失（TRD）。在这项研究中，我们结合了物理和遗传检测手段来研究TRD的机制。首先，为了区分几种重组途径和溶核途径，我们开发了一种新颖的物理分析方法，其中 Hae III限制性酶切位点位于端粒内。随后测试了特定端粒在TRD期间端粒之间的 Hae III位点移动和 Hae III位点保留。其次，遗传分析表明， RAD50 和 MRE11 中的突变会抑制TRD。但是，TRD独立于Rap1p C末端结构域，后者是端粒大小控制的中央调节剂。我们的结果提供了证据，表明TRD是染色质内删除过程，其中最末端附近的序列侵入末端-远端序列并切除中间的序列。我们提出，Mre11p-Rad50p-Xrs2p复合体可能通过末端加工或染色质结构改变，为链入侵准备了侵入的端粒突出端。

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