ArticlePLoS genetics2013
A role for the malignant brain tumour (MBT) domain protein LIN-61 in DNA double-strand break repair by homologous recombination.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- The DREAM complex functions as conserved master regulator of somatic DNA-repair capacities.Nature structural & molecular biology · 2023Article
- DNA repair, recombination, and damage signaling.Genetics · 2022Review
- Helicase Q promotes homology-driven DNA double-strand break repair and prevents tandem duplications.Nature communications · 2021Article
- Mechanism of mitotic recombination: insights from C. elegans.Current opinion in genetics & development · 2021Review
- Argonaute NRDE-3 and MBT domain protein LIN-61 redundantly recruit an H3K9me3 HMT to prevent embryonic lethality and transposon expression.Genes & development · 2021Article
- BRCA1-associated structural variations are a consequence of polymerase theta-mediated end-joining.Nature communications · 2020Article
- NADNature communications · 2019Article
- ALG-2/AGO-DependentGenetics · 2019Article
- A simple answer to complex questions: Caenorhabditis elegans as an experimental model for examining the DNA damage response and disease genes.Journal of cellular physiology · 2018Review
- Repressive Chromatin inGenetics · 2018Review
- Article
- JMJD-5/KDM8 regulates H3K36me2 and is required for late steps of homologous recombination and genome integrity.PLoS genetics · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malignant brain tumour (MBT) domain proteins are transcriptional repressors that function within Polycomb complexes. Some MBT genes are tumour suppressors, but how they prevent tumourigenesis is unknown. The Caenorhabditis elegans MBT protein LIN-61 is a member of the synMuvB chromatin-remodelling proteins that control vulval development. Here we report a new role for LIN-61: it protects the genome by promoting homologous recombination (HR) for the repair of DNA double-strand breaks (DSBs). lin-61 mutants manifest numerous problems associated with defective HR in germ and somatic cells but remain proficient in meiotic recombination. They are hypersensitive to ionizing radiation and interstrand crosslinks but not UV light. Using a novel reporter system that monitors repair of a defined DSB in C. elegans somatic cells, we show that LIN-61 contributes to HR. The involvement of this MBT protein in HR raises the possibility that MBT-deficient tumours may also have defective DSB repair.
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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.