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CST-Polα/Primase：第二 telomere 维持机器。

CST-Polα/Primase: the second telomere maintenance machine.

机构信息

Laboratory for Cell Biology and Genetics, The Rockefeller University, New York, New York 10065, USA.

Laboratory for Cell Biology and Genetics, The Rockefeller University, New York, New York 10065, USA

出版信息

Genes Dev. 2023 Jul 1;37(13-14):555-569. doi: 10.1101/gad.350479.123. Epub 2023 Jul 26.

DOI:10.1101/gad.350479.123
PMID:37495394
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10499019/
Abstract

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.

摘要

几十年来，人们已经知道端粒酶可以延伸线性真核染色体的 3' 端，并根据其 RNA 中的模板来决定端粒重复序列。然而，端粒酶并不能减轻染色体 5' 端由于滞后链 DNA 合成和核酸酶处理而导致的序列丢失。因此，需要第二种酶来保持端粒完整：与 Ctc1-Stn1-Ten1（CST）结合的 DNA 聚合酶 α/引发酶。CST-Polα/引发酶通过填补反应来维持端粒，从而在 5' 端补充丢失的序列。CST 不仅通过阻止端粒酶使端粒过长来维持端粒，还通过控制端粒酶来决定端粒的长度。本文讨论了关于哺乳动物 CST-Polα/引发酶的进化、结构、功能和募集的最新数据，重点介绍了该复合物和端粒长度控制在人类疾病中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d6f/10499019/1c41ddb5c493/555f06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d6f/10499019/8e4b6d07cde9/555f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d6f/10499019/75ea72bfc653/555f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d6f/10499019/513ba50f31d7/555f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d6f/10499019/ad40a1b5cfdf/555f04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d6f/10499019/fe7d0a97f132/555f05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d6f/10499019/1c41ddb5c493/555f06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d6f/10499019/8e4b6d07cde9/555f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d6f/10499019/75ea72bfc653/555f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d6f/10499019/513ba50f31d7/555f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d6f/10499019/ad40a1b5cfdf/555f04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d6f/10499019/fe7d0a97f132/555f05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d6f/10499019/1c41ddb5c493/555f06.jpg

相似文献

[1]
CST-Polα/Primase: the second telomere maintenance machine.

Genes Dev. 2023-7-1

[2]
CST-polymerase α-primase solves a second telomere end-replication problem.

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[3]
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Cell. 2024-7-11

[4]
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[5]
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[6]
Pol α-primase dependent nuclear localization of the mammalian CST complex.

Commun Biol. 2021-3-17

[7]
POT1 recruits and regulates CST-Polα/Primase at human telomeres.

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[8]
Models for human telomere C-strand fill-in by CST-Polα-primase.

Trends Biochem Sci. 2023-10

[9]
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[10]
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引用本文的文献

[1]
Distinct mechanisms underlying extrachromosomal telomere DNA generation in ALT cancers.

Nucleic Acids Res. 2025-8-11

[2]
Conserved and unique features of terminal telomeric sequences in ALT-positive cancer cells.

Elife. 2025-8-1

[3]
DNA polymerase α-primase can function as a translesion DNA polymerase.

bioRxiv. 2025-7-2

[4]
Conserved and Unique Features of Terminal Telomeric Sequences in ALT-Positive Cancer Cells.

bioRxiv. 2025-6-2

[5]
The - Mutant Provides New Insight into the Impacts of Telomeric Cdc13-Stn1-Ten1 Dysfunction on Cell Cycle Progression.

Cells. 2025-5-26

[6]
The yeast CST and Polα/primase complexes act in concert to ensure proper telomere maintenance and protection.

Nucleic Acids Res. 2025-4-10

[7]
Rapid dynamics allow the low-abundance RTEL1 helicase to promote telomere replication.

Nucleic Acids Res. 2025-2-27

[8]
Communication between DNA polymerases and Replication Protein A within the archaeal replisome.

Nat Commun. 2024-12-30

[9]
Identification of alternative lengthening of telomeres-related genes prognosis model in hepatocellular carcinoma.

BMC Cancer. 2024-11-11

[10]
Telomere maintenance and the DNA damage response: a paradoxical alliance.

Front Cell Dev Biol. 2024-10-17

本文引用的文献

[1]
RPA engages telomeric G-quadruplexes more effectively than CST.

Nucleic Acids Res. 2023-6-9

[2]
DNA-binding mechanism and evolution of replication protein A.

Nat Commun. 2023-4-22

[3]
CTC1 OB-B interaction with TPP1 terminates telomerase and prevents telomere overextension.

Nucleic Acids Res. 2023-6-9

[4]
Heritable defects in telomere and mitotic function selectively predispose to sarcomas.

Science. 2023-1-20

[5]
Dyskeratosis congenita and telomere biology disorders.

Hematology Am Soc Hematol Educ Program. 2022-12-9

[6]
CST/Polα/primase-mediated fill-in synthesis at DSBs.

Cell Cycle. 2023-2

[7]
Telomerase structural biology comes of age.

Curr Opin Struct Biol. 2022-10

[8]
Shelterin is a dimeric complex with extensive structural heterogeneity.

Proc Natl Acad Sci U S A. 2022-8-2

[9]
Reconstitution of a telomeric replicon organized by CST.

Nature. 2022-8

[10]
Structure of Tetrahymena telomerase-bound CST with polymerase α-primase.

Nature. 2022-8

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