ArticleMolecular and cellular biology2006
Regulation of gross chromosomal rearrangements by ubiquitin and SUMO ligases in Saccharomyces cerevisiae.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed.
- Cell Type Specific Suppression of Hyper-Recombination by Human RAD18 Is Linked to Proliferating Cell Nuclear Antigen K164 Ubiquitination.Biomolecules · 2025Article
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- Mgs1 function at G-quadruplex structures during DNA replication.Current genetics · 2021Review
- Non-recombinogenic roles for Rad52 in translesion synthesis during DNA damage tolerance.EMBO reports · 2021Article
- The HLTF-PARP1 interaction in the progression and stability of damaged replication forks caused by methyl methanesulfonate.Oncogenesis · 2020Article
- Prevention of unwanted recombination at damaged replication forks.Current genetics · 2020Review
- EssentialProceedings of the National Academy of Sciences of the United States of America · 2019Article
- The PCNA unloader Elg1 promotes recombination at collapsed replication forks in fission yeast.eLife · 2019Article
- Cooperation between non-essential DNA polymerases contributes to genome stability in Saccharomyces cerevisiae.DNA repair · 2019Article
- A Lysine Desert Protects a Novel Domain in the Slx5-Slx8 SUMO Targeted Ub Ligase To Maintain Sumoylation Levels inGenetics · 2017Article
- Pathways and Mechanisms that Prevent Genome Instability inGenetics · 2017Review
- BothAIMS genetics · 2017Article
- A Checkpoint-Related Function of the MCM Replicative Helicase Is Required to Avert Accumulation of RNA:DNA Hybrids during S-phase and Ensuing DSBs during G2/M.PLoS genetics · 2016Article
- Balancing self-renewal against genome preservation in stem cells: How do they manage to have the cake and eat it too?Cellular and molecular life sciences : CMLS · 2016Review
- A genetic network that suppresses genome rearrangements in Saccharomyces cerevisiae and contains defects in cancers.Nature communications · 2016Article
- Genetic Interactions Implicating Postreplicative Repair in Okazaki Fragment Processing.PLoS genetics · 2015Article
- Local regulation of the Srs2 helicase by the SUMO-like domain protein Esc2 promotes recombination at sites of stalled replication.Genes & development · 2015Article
- Yeast Assay Highlights the Intrinsic Genomic Instability of Human PML Intron 6 over Intron 3 and the Role of Replication Fork Proteins.PloS one · 2015Article
- Increased meiotic crossovers and reduced genome stability in absence of Schizosaccharomyces pombe Rad16 (XPF).Genetics · 2014Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Gross chromosomal rearrangements (GCRs) are frequently observed in many cancers. Previously, we showed that inactivation of Rad5 or Rad18, ubiquitin ligases (E3) targeting for proliferating cell nuclear antigen (PCNA), increases the de novo telomere addition type of GCR (S. Smith, J. Y. Hwang, S. Banerjee, A. Majeed, A. Gupta, and K. Myung, Proc. Natl. Acad. Sci. USA 101:9039-9044, 2004). GCR suppression by Rad5 and Rad18 appears to be exerted by the RAD5-dependent error-free mode of bypass DNA repair. In contrast, Siz1 SUMO ligase and another ubiquitin ligase, Bre1, which target for PCNA and histone H2B, respectively, have GCR-supporting activities. Inactivation of homologous recombination (HR) proteins or the helicase Srs2 reduces GCR rates elevated by the rad5 or rad18 mutation. GCRs are therefore likely to be produced through the restrained recruitment of an HR pathway to stalled DNA replication forks. Since this HR pathway is compatible with Srs2, it is not a conventional form of recombinational pathway. Lastly, we demonstrate that selection of proper DNA repair pathways to stalled DNA replication forks is controlled by the Mec1-dependent checkpoint and is executed by cooperative functions of Siz1 and Srs2. We propose a mechanism for how defects in these proteins could lead to diverse outcomes (proper repair or GCR formation) through different regulation of DNA repair machinery.
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