Intrachromatid excision of telomeric DNA as a mechanism for telomere size control in Saccharomyces cerevisiae
Intrachromatid excision of telomeric DNA as a mechanism for telomere size control in Saccharomyces cerevisiae
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DOI：
10.1128/mcb.21.19.6559-6573.2001
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发表时间：
2001-10-01
影响因子：
5.3
通讯作者：
Lustig, AJ
中科院分区：
文献类型：
--
作者：
Bucholc, M;Park, Y;Lustig, AJ
我们以前已经确定了一个过程中的酵母酿酒酵母，导致在几代内的收缩伸长端粒的野生型长度。我们将这一过程称为端粒快速缺失（TRD）。在这项研究中，我们使用物理和遗传分析相结合，以探讨TRD的机制。首先，为了区分几种重组和溶核途径，我们开发了一种新的物理检测方法，其中HaeIII限制性位点位于端粒道内。随后检测了特定端粒的HaeIII位点在端粒之间的移动和TRD期间HaeIII位点的保留。其次，遗传分析表明，RAD 50和MRE 11的突变抑制TRD。然而，TRD是独立的Rap 1 p C-末端结构域，端粒大小控制的中央调节器。我们的研究结果提供了证据表明，TRD是一个染色体内缺失的过程中，接近极端末端的序列侵入末端-远端序列和切除间插序列。我们建议，Mre 11 p-Rad 50 p-Xrs 2 p复合物准备入侵端粒悬垂链入侵，可能是通过末端加工或通过改变染色质结构。
We have previously identified a process in the yeast Saccharomyces 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 in RAD50 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.