Previous models suggested that regulation of telomere length in Saccharomyces cerevisiae by Tel1(ATM) and Mec1(ATR) would parallel the established pathways regulating the DNA damage response. Here, we provide evidence that telomere length regulation differs from the DNA damage response in both the Tel1 and Mec1 pathways. We found that Rad53 mediates a Mec1 telomere length regulation pathway but is dispensable for Tel1 telomere length regulation, whereas in the DNA damage response, Rad53 is regulated by both Mec1 and Tel1 Using epistasis analysis with a Tel1 hypermorphic allele, Tel1-hy909, we found that the MRX complex is not required downstream of Tel1 for telomere elongation but is required downstream of Tel1 for the DNA damage response. Our data suggest that nucleolytic telomere end processing is not a required step for telomerase to elongate telomeres.

中文翻译：

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MRX 复合物激活的 Tel1 足以调节端粒长度，但不足以调节酿酒酵母的 DNA 损伤反应。

先前的模型表明， Tel1(ATM) 和 Mec1(ATR) 对酿酒酵母中端粒长度的调节与已建立的调节 DNA 损伤反应的途径平行。在这里，我们提供的证据表明端粒长度调节与 Tel1 和 Mec1 途径中的 DNA 损伤反应不同。我们发现Rad53介导Mec1端粒长度调节途径，但对于Tel1端粒长度调节是可有可无的，而在DNA损伤反应中，Rad53同时受到Mec1和Tel1的调节。使用Tel1超态等位基因Tel1-hy909的上位性分析，我们发现Tel1 下游端粒延长不需要 MRX 复合物，但 DNA 损伤反应需要 Tel1 下游 MRX 复合物。我们的数据表明，溶核端粒末端加工不是端粒酶延长端粒的必要步骤。