ArticleNucleic acids research2013
Trypanosoma brucei BRCA2 acts in a life cycle-specific genome stability process and dictates BRC repeat number-dependent RAD51 subnuclear dynamics.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- De Novo Assembly of the Trypanosoma congolense Genome Reveals an Organization Influenced by Antigenic Variation but Distinct from Trypanosoma brucei.Genome biology and evolution · 2026Article
- Specialized RNA decay fine-tunes monogenic antigen expression in Trypanosoma brucei.Nature microbiology · 2026Article
- Nanopore sequencing reveals that DNA replication compartmentalisation dictates genome stability and instability in Trypanosoma brucei.Nature communications · 2025Article
- RAD51-mediated R-loop formation acts to repair transcription-associated DNA breaks driving antigenic variation inProceedings of the National Academy of Sciences of the United States of America · 2023Article
- The MRN complex promotes DNA repair by homologous recombination and restrains antigenic variation in African trypanosomes.Nucleic acids research · 2021Article
- Conditional knockout of RAD51-related genes in Leishmania major reveals a critical role for homologous recombination during genome replication.PLoS genetics · 2020Article
- Trypanosoma brucei ATR Links DNA Damage Signaling during Antigenic Variation with Regulation of RNA Polymerase I-Transcribed Surface Antigens.Cell reports · 2020Article
- Escaping the immune system by DNA repair and recombination in African trypanosomes.Open biology · 2019Review
- Article
- Emerging challenges in understanding trypanosome antigenic variation.Emerging topics in life sciences · 2017Article
- Does DNA replication direct locus-specific recombination during host immune evasion by antigenic variation in the African trypanosome?Current genetics · 2017Review
- Article
- The Knowns Unknowns: Exploring the Homologous Recombination Repair Pathway in Toxoplasma gondii.Frontiers in microbiology · 2016Review
- Molecular control of irreversible bistability during trypanosome developmental commitment.The Journal of cell biology · 2015Article
- Cancer in the parasitic protozoans Trypanosoma brucei and Toxoplasma gondii.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Distinct Phenotypes Caused by Mutation of MSH2 in Trypanosome Insect and Mammalian Life Cycle Forms Are Associated with Parasite Adaptation to Oxidative Stress.PLoS neglected tropical diseases · 2015Article
- DNA repair pathways in trypanosomatids: from DNA repair to drug resistance.Microbiology and molecular biology reviews : MMBR · 2014Review
- Antigenic variation in African trypanosomes: the importance of chromosomal and nuclear context in VSG expression control.Cellular microbiology · 2013Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Trypanosoma brucei survives in mammals through antigenic variation, which is driven by RAD51-directed homologous recombination of Variant Surface Glycoproteins (VSG) genes, most of which reside in a subtelomeric repository of >1000 silent genes. A key regulator of RAD51 is BRCA2, which in T. brucei contains a dramatic expansion of a motif that mediates interaction with RAD51, termed the BRC repeats. BRCA2 mutants were made in both tsetse fly-derived and mammal-derived T. brucei, and we show that BRCA2 loss has less impact on the health of the former. In addition, we find that genome instability, a hallmark of BRCA2 loss in other organisms, is only seen in mammal-derived T. brucei. By generating cells expressing BRCA2 variants with altered BRC repeat numbers, we show that the BRC repeat expansion is crucial for RAD51 subnuclear dynamics after DNA damage. Finally, we document surprisingly limited co-localization of BRCA2 and RAD51 in the T. brucei nucleus, and we show that BRCA2 mutants display aberrant cell division, revealing a function distinct from BRC-mediated RAD51 interaction. We propose that BRCA2 acts to maintain the huge VSG repository of T. brucei, and this function has necessitated the evolution of extensive RAD51 interaction via the BRC repeats, allowing re-localization of the recombinase to general genome damage when needed.
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Registered trials
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