ArticleNucleic acids research2014
Malaria parasites utilize both homologous recombination and alternative end joining pathways to maintain genome integrity.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 123 citations in OpenAlex.
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- Replication stress increases de novo CNVs across the malaria parasite genome.Nucleic acids research · 2026Article
- The impact of Iso-mukaadial acetate on Plasmodium falciparum transcriptional gene regulation.Scientific reports · 2025Article
- Plasmodium falciparum DNA repair dynamics reveal unique roles for TLS polymerases and PfRad51 in genome diversification.Nucleic acids research · 2025Article
- Replication stress increases de novo CNVs across the malaria parasite genome.bioRxiv : the preprint server for biology · 2025Article
- A CRISPR homing screen finds a chloroquine resistance transporter-like protein of the Plasmodium oocyst essential for mosquito transmission of malaria.Nature communications · 2025Article
- A scaleable inducible knockout system for studying essential gene function in the malaria parasite.Nucleic acids research · 2025Article
- A scalable CRISPR-Cas9 gene editing system facilitates CRISPR screens in the malaria parasite Plasmodium berghei.Nucleic acids research · 2025Article
- Applications of CRISPR in Parasitology.Current pharmaceutical biotechnology · 2025Review
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- Evaluation of topotecan and 10-hydroxycamptothecin on Toxoplasma gondii: Implications on baseline DNA damage and repair efficiency.International journal for parasitology. Drugs and drug resistance · 2023Article
- Effects of the G-quadruplex-binding drugs quarfloxin and CX-5461 on the malaria parasite Plasmodium falciparum.International journal for parasitology. Drugs and drug resistance · 2023Article
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- Uncovering the role of Rad51 in homologous recombination-mediated antigenic diversification in the human malaria parasiteFrontiers in molecular biosciences · 2023Article
- CRISPR-Cas9: Taming protozoan parasites with bacterial scissor.Journal of parasitic diseases : official organ of the Indian Society for Parasitology · 2022Review
- Plasmodium berghei Brca2 is required for normal development and differentiation in mice and mosquitoes.Parasites & vectors · 2022Article
13 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 2 institutions in 1 country.
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Abstract
Malaria parasites replicate asexually within their mammalian hosts as haploid cells and are subject to DNA damage from the immune response and chemotherapeutic agents that can significantly disrupt genomic integrity. Examination of the annotated genome of the parasite Plasmodium falciparum identified genes encoding core proteins required for the homologous recombination (HR) pathway for repairing DNA double-strand breaks (DSBs), but surprisingly none of the components of the canonical non-homologous end joining (C-NHEJ) pathway were identified. To better understand how malaria parasites repair DSBs and maintain genome integrity, we modified the yeast I-SceI endonuclease system to generate inducible, site-specific DSBs within the parasite's genome. Analysis of repaired genomic DNA showed that parasites possess both a typical HR pathway resulting in gene conversion events as well as an end joining (EJ) pathway for repair of DSBs when no homologous sequence is available. The products of EJ were limited in number and identical products were observed in multiple independent experiments. The repair junctions frequently contained short insertions also found in the surrounding sequences, suggesting the possibility of a templated repair process. We propose that an alternative end-joining pathway rather than C-NHEJ, serves as a primary method for repairing DSBs in malaria parasites.
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