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Chl1 helicase contr...
Chl1 helicase controls replication fork progression by regulating dNTP pools
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- Batté, Amandine (författare)
- Department of Human Genetics, Leiden University Medical Center, Leiden, Netherlands
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- van der Horst, Sophie C. (författare)
- Department of Human Genetics, Leiden University Medical Center, Leiden, Netherlands
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- Tittel-Elmer, Mireille (författare)
- Department of Human Genetics, Leiden University Medical Center, Leiden, Netherlands; Electrical Engineering, Mathematics and Computer Science, Delft University of Technology, Delft, Netherlands
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- Sun, Su Ming (författare)
- Department of Human Genetics, Leiden University Medical Center, Leiden, Netherlands
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- Sharma, Sushma (författare)
- Umeå universitet,Institutionen för medicinsk kemi och biofysik
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- van Leeuwen, Jolanda (författare)
- Center for Integrative Genomics, Université de Lausanne, Switzerland
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- Chabes, Andrei, Professor (författare)
- Umeå universitet,Institutionen för medicinsk kemi och biofysik
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- van Attikum, Haico (författare)
- Department of Human Genetics, Leiden University Medical Center, Leiden, Netherlands
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(creator_code:org_t)
- 2022-01-11
- 2022
- Engelska.
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Ingår i: Life Science Alliance. - : Life Science Alliance, LLC. - 2575-1077. ; 5:4
- Relaterad länk:
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https://doi.org/10.2...
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https://umu.diva-por... (primary) (Raw object)
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https://www.life-sci...
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https://urn.kb.se/re...
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https://doi.org/10.2...
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Abstract
Ämnesord
Stäng
- Eukaryotic cells have evolved a replication stress response that helps to overcome stalled/collapsed replication forks and ensure proper DNA replication. The replication checkpoint protein Mrc1 plays important roles in these processes, although its functional interactions are not fully understood. Here, we show that MRC1 negatively interacts with CHL1, which encodes the helicase protein Chl1, suggesting distinct roles for these factors during the replication stress response. Indeed, whereas Mrc1 is known to facilitate the restart of stalled replication forks, we uncovered that Chl1 controls replication fork rate under replication stress conditions. Chl1 loss leads to increased RNR1 gene expression and dNTP levels at the onset of S phase likely without activating the DNA damage response. This in turn impairs the formation of RPA-coated ssDNA and subsequent checkpoint activation. Thus, the Chl1 helicase affects RPA-dependent checkpoint activation in response to replication fork arrest by ensuring proper intracellular dNTP levels, thereby controlling replication fork progression under replication stress conditions.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Cell- och molekylärbiologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Cell and Molecular Biology (hsv//eng)
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