ArticleFrontiers in genetics2013
BLM SUMOylation regulates ssDNA accumulation at stalled replication forks.
Article in Frontiers in genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 35 citations in OpenAlex.
- GNL3 SUMOylation is essential for DNA double-strand break repair by homologous recombination.Nature communications · 2026Article
- SLX4IP limits replication stress globally and at ALT telomeres.The EMBO journal · 2026Article
- Solubility based mechanistic profiling of combinatorial drug therapy.Nature communications · 2026Article
- Multifaceted roles of SUMO in DNA metabolism.Nucleus (Austin, Tex.) · 2024Review
- BLM Sumoylation Is Required for Replication Stability and Normal Fork Velocity During DNA Replication.Frontiers in molecular biosciences · 2022Article
- 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
- Functions of BLM Helicase in Cells: Is It Acting Like a Double-Edged Sword?Frontiers in genetics · 2021Review
- Vpu modulates DNA repair to suppress innate sensing and hyper-integration of HIV-1.Nature microbiology · 2020Article
- The Promyelocytic Leukemia Protein facilitates human herpesvirus 6B chromosomal integration, immediate-early 1 protein multiSUMOylation and its localization at telomeres.PLoS pathogens · 2020Article
- Intricate SUMO-based control of the homologous recombination machinery.Genes & development · 2019Review
- Cyclin E Overexpression Sensitizes Triple-Negative Breast Cancer to Wee1 Kinase Inhibition.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- RECQ helicase disease and related progeroid syndromes: RECQ2018 meeting.Mechanisms of ageing and development · 2018Review
- A tri-serine cluster within the topoisomerase IIα-interaction domain of the BLM helicase is required for regulating chromosome breakage in human cells.Human molecular genetics · 2018Article
- Article
- Genetic Evidence for Roles of Yeast Mitotic Cyclins at Single-Stranded Gaps Created by DNA Replication.G3 (Bethesda, Md.) · 2018Article
- Dynamics of RIF1 SUMOylation is regulated by PIAS4 in the maintenance of Genomic Stability.Scientific reports · 2017Article
- SUMO and the robustness of cancer.Nature reviews. Cancer · 2017Review
- Bloom's Syndrome: Clinical Spectrum, Molecular Pathogenesis, and Cancer Predisposition.Molecular syndromology · 2017Review
- Bloom's syndrome: Why not premature aging?: A comparison of the BLM and WRN helicases.Ageing research reviews · 2017Review
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
Polymerase stalling results in uncoupling of DNA polymerase and the replicative helicase, which generates single-stranded DNA (ssDNA). After stalling, RAD51 accumulates at stalled replication forks to stabilize the fork and to repair by homologous recombination (HR) double-strand breaks (DSBs) that accumulate there. We showed recently that SUMO modification of the BLM helicase is required in order for RAD51 to accumulate at stalled forks. In order to investigate how BLM SUMOylation controls RAD51 accumulation, we characterized the function of HR proteins and ssDNA-binding protein RPA in cells that stably expressed either normal BLM (BLM+) or SUMO-mutant BLM (SM-BLM). In HU-treated SM-BLM cells, mediators BRCA2 and RAD52, which normally substitute RAD51 for RPA on ssDNA, failed to accumulate normally at stalled forks; instead, excess RPA accumulated. SM-BLM cells also exhibited higher levels of HU-induced chromatin-bound RPA than BLM+ cells did. The excess RPA did not result from excessive intrinsic BLM helicase activity, because in vitro SUMOylated BLM unwound similar amounts of replication-fork substrate as unSUMOylated BLM. Nor did BLM SUMOylation inhibit binding of RPA to BLM in vitro; however, in immunoprecipitation experiments, more BLM-RPA complex formed in HU-treated SM-BLM cells, indicating that BLM SUMOylation controls the amount of BLM-RPA complex normally formed at stalled forks. Together, these results showed that BLM SUMOylation regulates the amount of ssDNA that accumulates during polymerase stalling. We conclude that BLM SUMOylation functions as a licensing mechanism that permits and regulates HR at damaged replication forks.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.