To examine the established link between DNA replication and telomere length, we tested whether firing of telomeric origins would cause telomere lengthening. We found that RIF1 mutants that block Protein Phosphatase 1 (PP1) binding activated telomeric origins but did not elongate telomeres. In a second approach, we found overexpression of ∆N-Dbf4 and Cdc7 increased DDK activity and activated telomeric origins, yet telomere length was unchanged. We tested a third mechanism to activate origins using the sld3-A mcm5-bob1 mutant that de-regulates the pre-replication complex, and again saw no change in telomere length. Finally, we tested whether mutations in RIF1 that cause telomere elongation would affect origin firing. We found that neither rif1-∆1322 nor rif1HOOK affected firing of telomeric origins. We conclude that telomeric origin firing does not cause telomere elongation, and the role of Rif1 in regulating origin firing is separable from its role in regulating telomere length.

中文翻译：

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Rif1 在端粒长度调节中的作用与其在起源发射中的作用是分开的

为了检查 DNA 复制和端粒长度之间已建立的联系，我们测试了端粒起源的激发是否会导致端粒延长。我们发现阻断蛋白磷酸酶 1 (PP1) 结合的 RIF1 突变体激活了端粒起源，但没有延长端粒。在第二种方法中，我们发现 ∆N-Dbf4 和 Cdc7 的过度表达增加了 DDK 活性并激活了端粒起源，但端粒长度没有变化。我们使用 sld3-A mcm5-bob1 突变体测试了第三种激活起源的机制，该突变体解除了复制前复合体的调节，再次看到端粒长度没有变化。最后，我们测试了导致端粒伸长的 RIF1 突变是否会影响起源放电。我们发现 rif1-∆1322 和 rif1HOOK 都不影响端粒起源的发射。