ArticlePLoS genetics2018
SUMO E3 ligase Mms21 prevents spontaneous DNA damage induced genome rearrangements.
Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Ligase-dependent and independent functions of the C-terminus of Mms21 contribute to optimal growth and genome stability inMolecular biology of the cell · 2026Article
- Double-strand breaks induce inverted duplication chromosome rearrangements by a DNA polymerase δ-dependent mechanism.Nature communications · 2023Article
- SUMO-activated target traps (SATTs) enable the identification of a comprehensive E3-specific SUMO proteome.Science advances · 2023Article
- The multi-functional Smc5/6 complex in genome protection and disease.Nature structural & molecular biology · 2023Review
- Site-specific MCM sumoylation prevents genome rearrangements by controlling origin-bound MCM.PLoS genetics · 2022Article
- Acute ethanol stress induces sumoylation of conserved chromatin structural proteins inMolecular biology of the cell · 2021Article
- Shared and distinct roles of Esc2 and Mms21 in suppressing genome rearrangements and regulating intracellular sumoylation.PloS one · 2021Article
- Mechanisms underlying genome instability mediated by formation of foldback inversions ineLife · 2020Article
- Review
- Rescue of collapsed replication forks is dependent on NSMCE2 to prevent mitotic DNA damage.PLoS genetics · 2019Article
- Guidelines for DNA recombination and repair studies: Cellular assays of DNA repair pathways.Microbial cell (Graz, Austria) · 2019Review
- SMC5/6: Multifunctional Player in Replication.Genes · 2018Review
- The plasma peptides of ovarian cancer.Clinical proteomics · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Mms21, a subunit of the Smc5/6 complex, possesses an E3 ligase activity for the Small Ubiquitin-like MOdifier (SUMO). Here we show that the mms21-CH mutation, which inactivates Mms21 ligase activity, causes increased accumulation of gross chromosomal rearrangements (GCRs) selected in the dGCR assay. These dGCRs are formed by non-allelic homologous recombination between divergent DNA sequences mediated by Rad52-, Rrm3- and Pol32-dependent break-induced replication. Combining mms21-CH with sgs1Δ caused a synergistic increase in GCRs rates, indicating the distinct roles of Mms21 and Sgs1 in suppressing GCRs. The mms21-CH mutation also caused increased rates of accumulating uGCRs mediated by breakpoints in unique sequences as revealed by whole genome sequencing. Consistent with the accumulation of endogenous DNA lesions, mms21-CH mutants accumulate increased levels of spontaneous Rad52 and Ddc2 foci and had a hyper-activated DNA damage checkpoint. Together, these findings support that Mms21 prevents the accumulation of spontaneous DNA lesions that cause diverse GCRs.
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Registered trials
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.