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TFIIH moonlighting at telomeres

Although telomeres are essential for chromosome stability, they represent fragile structures in our genome. Telomere shortening occurs during aging in cells lacking telomerase due to the end replication problem. In addition, recent work uncovered that the bulk of telomeric DNA poses severe hurdles f...

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Detalles Bibliográficos
Autores principales: Glousker, Galina, Lingner, Joachim
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cold Spring Harbor Laboratory Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9732908/
https://www.ncbi.nlm.nih.gov/pubmed/36347559
http://dx.doi.org/10.1101/gad.350140.122
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author Glousker, Galina
Lingner, Joachim
author_facet Glousker, Galina
Lingner, Joachim
author_sort Glousker, Galina
collection PubMed
description Although telomeres are essential for chromosome stability, they represent fragile structures in our genome. Telomere shortening occurs during aging in cells lacking telomerase due to the end replication problem. In addition, recent work uncovered that the bulk of telomeric DNA poses severe hurdles for the semiconservative DNA replication machinery, requiring the assistance of an increasing number of specialized factors that prevent accidental telomere loss or damage events. In this issue of Genes & Development, Yang and colleagues (pp. 956–969) discover that TFIIH, a basic component of the PolII transcription initiation and nucleotide excision repair machinery, facilitates telomere replication. TFIIH is recruited to telomeres by the shelterin component TRF1, taking on at telomeres a moonlighting function.
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spelling pubmed-97329082023-03-01 TFIIH moonlighting at telomeres Glousker, Galina Lingner, Joachim Genes Dev Outlook Although telomeres are essential for chromosome stability, they represent fragile structures in our genome. Telomere shortening occurs during aging in cells lacking telomerase due to the end replication problem. In addition, recent work uncovered that the bulk of telomeric DNA poses severe hurdles for the semiconservative DNA replication machinery, requiring the assistance of an increasing number of specialized factors that prevent accidental telomere loss or damage events. In this issue of Genes & Development, Yang and colleagues (pp. 956–969) discover that TFIIH, a basic component of the PolII transcription initiation and nucleotide excision repair machinery, facilitates telomere replication. TFIIH is recruited to telomeres by the shelterin component TRF1, taking on at telomeres a moonlighting function. Cold Spring Harbor Laboratory Press 2022-09-01 /pmc/articles/PMC9732908/ /pubmed/36347559 http://dx.doi.org/10.1101/gad.350140.122 Text en © 2022 Glousker and Lingner; Published by Cold Spring Harbor Laboratory Press https://creativecommons.org/licenses/by-nc/4.0/This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) .
spellingShingle Outlook
Glousker, Galina
Lingner, Joachim
TFIIH moonlighting at telomeres
title TFIIH moonlighting at telomeres
title_full TFIIH moonlighting at telomeres
title_fullStr TFIIH moonlighting at telomeres
title_full_unstemmed TFIIH moonlighting at telomeres
title_short TFIIH moonlighting at telomeres
title_sort tfiih moonlighting at telomeres
topic Outlook
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9732908/
https://www.ncbi.nlm.nih.gov/pubmed/36347559
http://dx.doi.org/10.1101/gad.350140.122
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