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Your search keyword '"van den Berg, Debbie L. C."' showing total 2 results
Start Over Author "van den Berg, Debbie L. C." Journal nature cell biology
2 results on '"van den Berg, Debbie L. C."'

1. Transcription-coupled DNA–protein crosslink repair by CSB and CRL4CSA-mediated degradation

Author

van Sluis, Marjolein, Yu, Qing, van der Woude, Melanie, Gonzalo-Hansen, Camila, Dealy, Shannon C., Janssens, Roel C., Somsen, Hedda B., Ramadhin, Anisha R., Dekkers, Dick H. W., Wienecke, Hannah Lena, Demmers, Joris J. P. G., Raams, Anja, Davó-Martínez, Carlota, Llerena Schiffmacher, Diana A., van Toorn, Marvin, Häckes, David, Thijssen, Karen L., Zhou, Di, Lammers, Judith G., Pines, Alex, Vermeulen, Wim, Pothof, Joris, Demmers, Jeroen A. A., van den Berg, Debbie L. C., Lans, Hannes, and Marteijn, Jurgen A.

Published
2024
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2. The Williams syndrome transcription factor interacts with PCNA to target chromatin remodelling by ISWI to replication foci.

Author

Poot RA, Bozhenok L, van den Berg DL, Steffensen S, Ferreira F, Grimaldi M, Gilbert N, Ferreira J, and Varga-Weisz PD

Subjects
Adenosine Triphosphatases genetics, Adenosine Triphosphate metabolism, Chromatin genetics, Chromatin metabolism, Chromatin Assembly and Disassembly genetics, Chromobox Protein Homolog 5, Chromosomal Proteins, Non-Histone genetics, Chromosomal Proteins, Non-Histone metabolism, Chromosomes, Human, Pair 7 genetics, Genetic Markers genetics, HeLa Cells, Humans, Nuclear Proteins genetics, Nuclear Proteins metabolism, Proliferating Cell Nuclear Antigen genetics, RNA Interference, Transcription Factors genetics, Williams Syndrome metabolism, Adenosine Triphosphatases metabolism, Chromatin Assembly and Disassembly physiology, DNA Replication genetics, Proliferating Cell Nuclear Antigen metabolism, Transcription Factors metabolism, Williams Syndrome genetics
Abstract

Chromatin states have to be faithfully duplicated during DNA replication to maintain cell identity. It is unclear whether or how ATP-dependent chromatin-remodelling factors are involved in this process. Here we provide evidence that the Williams syndrome transcription factor (WSTF) is targeted to replication foci through direct interaction with the DNA clamp PCNA, an important coordinator of DNA and chromatin replication. WSTF, in turn, recruits imitation switch (ISWI)-type nucleosome-remodelling factor SNF2H to replication sites. These findings reveal a novel recruitment mechanism for ATP-dependent chromatin-remodelling factors that is fundamentally different from the previously documented targeting by sequence-specific transcriptional regulators. RNA-interference-mediated depletion of WSTF or SNF2H causes a compaction of newly replicated chromatin and increases the amount of heterochromatin markers, including HP1beta. This increase in the amount of HP1beta protein is mediated by progression through S phase and is not the result of an increase in HP1beta mRNA levels. We propose that the WSTF-ISWI complex has a role in the maintenance of chromatin structures during DNA replication.

Published
2004
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