It has been known for decades that telomerase extends the 3′ end of linear eukaryotic chromosomes and dictates the telomeric repeat sequence based on the template in its RNA. However, telomerase does not mitigate sequence loss at the 5′ ends of chromosomes, which results from lagging strand DNA synthesis and nucleolytic processing. Therefore, a second enzyme is needed to keep telomeres intact: DNA polymerase α/Primase bound to Ctc1–Stn1–Ten1 (CST). CST–Polα/Primase maintains telomeres through a fill-in reaction that replenishes the lost sequences at the 5′ ends. CST not only serves to maintain telomeres but also determines their length by keeping telomerase from overelongating telomeres. Here we discuss recent data on the evolution, structure, function, and recruitment of mammalian CST–Polα/Primase, highlighting the role of this complex and telomere length control in human disease.

中文翻译：

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CST–Polα/Primase：第二台端粒维护机器

几十年来，人们就知道端粒酶会延伸线性真核染色体的 3' 端，并根据其 RNA 中的模板决定端粒重复序列。然而，端粒酶并不能减轻染色体 5' 端的序列丢失，这是由滞后链 DNA 合成和溶核加工造成的。因此，需要第二种酶来保持端粒完整：DNA 聚合酶 α/Primase 与 Ctc1–Stn1–Ten1 (CST) 结合。CST-Polα/Primase 通过填充反应来补充 5' 端丢失的序列，从而维持端粒。CST 不仅可以维持端粒，还可以通过阻止端粒酶过度延长端粒来确定端粒长度。在这里，我们讨论有关哺乳动物 CST-Polα/Primase 的进化、结构、功能和招募的最新数据，强调这种复合体和端粒长度控制在人类疾病中的作用。