ArticlePLoS biology2009
SUMO modification regulates BLM and RAD51 interaction at damaged replication forks.
Article in PLoS biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 123 citations in OpenAlex.
- GNL3 SUMOylation is essential for DNA double-strand break repair by homologous recombination.Nature communications · 2026Article
- R-loops and D-loops: a delicate balance in genomic stability and instability.Cell communication and signaling : CCS · 2026Review
- SLX4IP limits replication stress globally and at ALT telomeres.The EMBO journal · 2026Article
- K63-linked ubiquitylation of RMI1 by RNF8 is essential to its recruitment to stalled forks.Cellular and molecular life sciences : CMLS · 2026Article
- DNA double strand break repair: a model of specificity and complexity in SUMO signalling.Essays in biochemistry · 2025Review
- Review
- SUMO promotes DNA repair protein collaboration to support alternative telomere lengthening in the absence of PML.Genes & development · 2024Article
- SUMO and the DNA damage response.Biochemical Society transactions · 2024Review
- PTEN-mediated dephosphorylation of 53BP1 confers cellular resistance to DNA damage in cancer cells.Molecular oncology · 2024Article
- SUMO Promotes DNA Repair Protein Collaboration to Support Alterative Telomere Lengthening in the Absence of PML.bioRxiv : the preprint server for biology · 2024Article
- PARP1 negatively regulates transcription of BLM through its interaction with HSP90AB1 in prostate cancer.Journal of translational medicine · 2023Article
- Comprehensive Interactome Mapping of the DNA Repair Scaffold SLX4 Using Proximity Labeling and Affinity Purification.Journal of proteome research · 2023Article
- Article
- DNA Double-Strand Breaks as Pathogenic Lesions in Neurological Disorders.International journal of molecular sciences · 2022Review
- TOPORS-mediated RAD51 SUMOylation facilitates homologous recombination repair.Nucleic acids research · 2022Article
- Post-Translational Modification of GPX4 is a Promising Target for Treating Ferroptosis-Related Diseases.Frontiers in molecular biosciences · 2022Review
- BLM Sumoylation Is Required for Replication Stability and Normal Fork Velocity During DNA Replication.Frontiers in molecular biosciences · 2022Article
- Rrp1 translocase and ubiquitin ligase activities restrict the genome destabilising effects of Rad51 in fission yeast.Nucleic acids research · 2021Article
- SUMOylation mediates CtIP's functions in DNA end resection and replication fork protection.Nucleic acids research · 2021Article
- RNF4 Regulates the BLM Helicase in Recovery From Replication Fork Collapse.Frontiers in genetics · 2021Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The gene mutated in Bloom's syndrome, BLM, is important in the repair of damaged replication forks, and it has both pro- and anti-recombinogenic roles in homologous recombination (HR). At damaged forks, BLM interacts with RAD51 recombinase, the essential enzyme in HR that catalyzes homology-dependent strand invasion. We have previously shown that defects in BLM modification by the small ubiquitin-related modifier (SUMO) cause increased gamma-H2AX foci. Because the increased gamma-H2AX could result from defective repair of spontaneous DNA damage, we hypothesized that SUMO modification regulates BLM's function in HR repair at damaged forks. To test this hypothesis, we treated cells that stably expressed a normal BLM (BLM+) or a SUMO-mutant BLM (SM-BLM) with hydroxyurea (HU) and examined the effects of stalled replication forks on RAD51 and its DNA repair functions. HU treatment generated excess gamma-H2AX in SM-BLM compared to BLM+ cells, consistent with a defect in replication-fork repair. SM-BLM cells accumulated increased numbers of DNA breaks and were hypersensitive to DNA damage. Importantly, HU treatment failed to induce sister-chromatid exchanges in SM-BLM cells compared to BLM+ cells, indicating a specific defect in HR repair and suggesting that RAD51 function could be compromised. Consistent with this hypothesis, RAD51 localization to HU-induced repair foci was impaired in SM-BLM cells. These data suggested that RAD51 might interact noncovalently with SUMO. We found that in vitro RAD51 interacts noncovalently with SUMO and that it interacts more efficiently with SUMO-modified BLM compared to unmodified BLM. These data suggest that SUMOylation controls the switch between BLM's pro- and anti-recombinogenic roles in HR. In the absence of BLM SUMOylation, BLM perturbs RAD51 localization at damaged replication forks and inhibits fork repair by HR. Conversely, BLM SUMOylation relieves its inhibitory effects on HR, and it promotes RAD51 function.
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