BOD1L Is Required to Suppress Deleterious Resection of Stressed Replication Forks
Open accessAbstract
Recognition and repair of damaged replication forks are essential to maintain genome stability and are coordinated by the combined action of the Fanconi anemia and homologous recombination pathways. These pathways are vital to protect stalled replication forks from uncontrolled nucleolytic activity, which otherwise causes irreparable genomic damage. Here, we identify BOD1L as a component of this fork protection pathway, which safeguards genome stability after replication stress. Loss of BOD1L confers exquisite cellular sensitivity to replication stress and uncontrolled resection of damaged replication forks, due to a failure to stabilize RAD51 at these forks. Blocking DNA2-dependent resection, or downregulation of the helicases BLM and FBH1, suppresses both catastrophic fork processing and the accumulation of chromosomal damage in BOD1L-deficient cells. Thus, our work implicates BOD1L as a critical regulator of genome integrity that restrains nucleolytic degradation of damaged replication forks.
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Micro3 showed similarities to HM_3, HM_4 but also expressed APOE, apoptosis associated genes XAF1, YWHAB, YWHAG, YWHAE, cell-cycle and cell division control genes CDK12, MIS18BP1, TAF1D, BOD1L1 and CCAR1.
“Micro3 showed similarities to HM_3, HM_4 phenotype but also expressed APOE, apoptosis associated genes XAF1, YWHAB, YWHAG, YWHAE encoding 14–3-3 protein subunits, cell-cycle and cell division control genes CDK12, MIS18BP1, TAF1D, BOD1L1 and CCAR1 [6, 30, 67].”
From Characterisation of premature cell senescence in Alzheimer's disease using single nuclear transcriptomics (2024) · cites this paper as [30]
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References 52 · Cited by 194
- Authors
- Higgs, M. R., Reynolds, J. J., Winczura, A., Blackford, A. N., Borel, V., Miller, E. S., Zlatanou, A., Nieminuszczy, J., Ryan, E. L., Davies, N. J., Stankovic, T., Boulton, S. J., Niedzwiedz, W., & Stewart, G. S.
- Affiliations
- University of Birmingham (GB)
- University of Oxford (GB)
- The Francis Crick Institute (GB)
- Corresponding author
- Stewart, Grant S.
- ORCID
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2015-08
- Volume
- 59
- Issue
- 3
- Pages
- 462-477
- ISSN
- 1097-2765 (ISSN-L)
- OpenAlex
- W1516566300
- Cited by
- 194
- References
- 52
- Citations by year
- 2026: 4 · 2025: 19 · 2024: 20 · 2023: 24 · 2022: 11 · 2021: 23 · 2020: 26 · 2019: 18 · 2018: 20 · 2017: 16 · 2016: 12 · 2015: 1
- FWCI
- 7.10
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Molecular Cell (publishedVersion)
- PubMed (publishedVersion)
- University of Birmingham Research Portal (University of Birmingham) (submittedVersion)
- Funders
- Wellcome Trust (104558, 104558/Z/14/Z)
- Francis Crick Institute (10048)
- Cancer Research UK (11581, 13030, 11224)
- Medical Research Council (MR/M009882/1)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA and Nucleic Acid Chemistry
- Keywords
- replication stress, genome stability, RAD51, DNA2, Fanconi anemia pathway, homologous recombination, BLM helicase, chromosomal damage
- MeSH terms
- Cell Line, Cell Survival, DNA Damage, DNA Replication, DNA Helicases, DNA-Binding Proteins, HeLa Cells, Humans, Genome, Human, Cell Cycle Proteins, Genomic Instability, Rad51 Recombinase, RecQ Helicases
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