WD40-repeat protein WDR18 collaborates with TopBP1 to facilitate DNA damage checkpoint signaling
Open accessAbstract
The genomes of all living organisms are exposed to a wide spectrum of insults. To maintain genomic integrity, eukaryotes have evolved an elaborate surveillance mechanism - DNA damage checkpoint signaling - to detect damaged DNA and to arrest cell cycle progression, allowing time to process and repair DNA damage. TopBP1 plays multiple roles in the regulation of DNA damage checkpoint signaling. However, the molecular mechanism of how TopBP1 regulates ATR-mediated Chk1 phosphorylation is poorly understood. In this communication, we demonstrate (1) that the Chk1 activation domain of TopBP1 is critical in response to several different types of DNA damage; (2) that WD40-repeat protein WDR18 associates with the C-terminus of TopBP1 in vitro and in vivo; (3) that the association between WDR18 and TopBP1 is required for AT70-induced Chk1 phosphorylation; (4) and that WDR18 itself is required for AT70-triggered Chk1 phosphorylation. In addition, WDR18 associates with Chk1 in vitro. The data suggest that WDR18 facilitates ATR-dependent Chk1 phosphorylation via interacting with both C-terminus of TopBP1 and Chk1. Our findings indicate that WDR18 is a bona fide checkpoint protein and that WDR18 works together with TopBP1 to promote DNA damage checkpoint signaling.
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Chk1 is phosphorylated at serine 345 by ATR in response to stalled DNA replication forks and DNA damage induced by UV, ionizing radiation, methyl methanesulfonate, mitomycin C, and hydrogen peroxide.
“As a critical player in DDR, Chk1 is phosphorylated at Serine 345 by ATR in response to stalled DNA replication forks and DNA damage induced by UV, IR, methyl methanesulfonate (MMS), mitomycin C (MMC), and hydrogen peroxide [85–90].”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [88]
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- Authors
- Yan, S., & Willis, J.
- Affiliations
- University of North Carolina at Charlotte (US)
- Corresponding author
- Yan, Shan
- ORCID
- Yan, Shan
- Venue
- Biochemical and Biophysical Research Communications
- Publisher
- Elsevier BV
- Published
- 2013-02
- Volume
- 431
- Issue
- 3
- Pages
- 466-471
- ISSN
- 0006-291X (ISSN-L)
- PMC
- PMC3577970
- OpenAlex
- W2094650649
- Cited by
- 16
- References
- 37
- Citations by year
- 2024: 2 · 2021: 2 · 2019: 2 · 2018: 1 · 2016: 1 · 2015: 3 · 2014: 4 · 2013: 1
- FWCI
- 1.34
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biochemical and Biophysical Research Communications (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- University of North Carolina at Charlotte
- NIGMS/NIH (R15 GM101571)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- TopBP1, Chk1 phosphorylation, ATR kinase, WD40 repeat proteins, protein-protein interaction, DNA damage response, genome stability
- MeSH terms
- Checkpoint Kinase 1, Animals, Carrier Proteins, DNA Damage, DNA-Binding Proteins, Oocytes, Phosphorylation, Protein Kinases, Xenopus laevis, Signal Transduction, Protein Structure, Tertiary, Xenopus Proteins, Intracellular Signaling Peptides and Proteins, Cell Cycle Checkpoints
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