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Mitotic bookmarking by transcription factors

Mitosis is accompanied by dramatic changes in chromatin organization and nuclear architecture. Transcription halts globally and most sequence-specific transcription factors and co-factors are ejected from mitotic chromatin. How then does the cell maintain its transcriptional identity throughout the...

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Detalles Bibliográficos
Autores principales: Kadauke, Stephan, Blobel, Gerd A
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3621617/
https://www.ncbi.nlm.nih.gov/pubmed/23547918
http://dx.doi.org/10.1186/1756-8935-6-6
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author Kadauke, Stephan
Blobel, Gerd A
author_facet Kadauke, Stephan
Blobel, Gerd A
author_sort Kadauke, Stephan
collection PubMed
description Mitosis is accompanied by dramatic changes in chromatin organization and nuclear architecture. Transcription halts globally and most sequence-specific transcription factors and co-factors are ejected from mitotic chromatin. How then does the cell maintain its transcriptional identity throughout the cell division cycle? It has become clear that not all traces of active transcription and gene repression are erased within mitotic chromatin. Many histone modifications are stable or only partially diminished throughout mitosis. In addition, some sequence-specific DNA binding factors have emerged that remain bound to select sites within mitotic chromatin, raising the possibility that they function to transmit regulatory information through the transcriptionally silent mitotic phase, a concept that has been termed “mitotic bookmarking.” Here we review recent approaches to studying potential bookmarking factors with regards to their mitotic partitioning, and summarize emerging ideas concerning the in vivo functions of mitotically bound nuclear factors.
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spelling pubmed-36216172013-04-10 Mitotic bookmarking by transcription factors Kadauke, Stephan Blobel, Gerd A Epigenetics Chromatin Review Mitosis is accompanied by dramatic changes in chromatin organization and nuclear architecture. Transcription halts globally and most sequence-specific transcription factors and co-factors are ejected from mitotic chromatin. How then does the cell maintain its transcriptional identity throughout the cell division cycle? It has become clear that not all traces of active transcription and gene repression are erased within mitotic chromatin. Many histone modifications are stable or only partially diminished throughout mitosis. In addition, some sequence-specific DNA binding factors have emerged that remain bound to select sites within mitotic chromatin, raising the possibility that they function to transmit regulatory information through the transcriptionally silent mitotic phase, a concept that has been termed “mitotic bookmarking.” Here we review recent approaches to studying potential bookmarking factors with regards to their mitotic partitioning, and summarize emerging ideas concerning the in vivo functions of mitotically bound nuclear factors. BioMed Central 2013-04-02 /pmc/articles/PMC3621617/ /pubmed/23547918 http://dx.doi.org/10.1186/1756-8935-6-6 Text en Copyright © 2013 Kadauke and Blobel; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Kadauke, Stephan
Blobel, Gerd A
Mitotic bookmarking by transcription factors
title Mitotic bookmarking by transcription factors
title_full Mitotic bookmarking by transcription factors
title_fullStr Mitotic bookmarking by transcription factors
title_full_unstemmed Mitotic bookmarking by transcription factors
title_short Mitotic bookmarking by transcription factors
title_sort mitotic bookmarking by transcription factors
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3621617/
https://www.ncbi.nlm.nih.gov/pubmed/23547918
http://dx.doi.org/10.1186/1756-8935-6-6
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