ArticleNucleic acids research2019
Complex DNA structures trigger copy number variation across the Plasmodium falciparum genome.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Replication stress increases de novo CNVs across the malaria parasite genome.Nucleic acids research · 2026Article
- Replication stress increases de novo CNVs across the malaria parasite genome.bioRxiv : the preprint server for biology · 2025Article
- Direct long-read visualization reveals hidden variation in GCH1 gene copy number and precise expansion steps.BMC genomics · 2025Article
- Low prevalence of copy number variation in pfmdr1 and pfpm2 in Plasmodium falciparum isolates from southern Angola.Malaria journal · 2025Article
- Systematic in vitro evolution inScience (New York, N.Y.) · 2024Article
- Direct long read visualization reveals metabolic interplay between two antimalarial drug targets.bioRxiv : the preprint server for biology · 2023Article
- DNA sequence features underlying large-scale duplications and deletions in human.Journal of applied genetics · 2022Article
- Whole Genome Sequencing Contributions and Challenges in Disease Reduction Focused on Malaria.Biology · 2022Review
- Single-cell sequencing of the small and AT-skewed genome of malaria parasites.Genome medicine · 2021Article
- The contribution of extrachromosomal DNA to genome plasticity in malaria parasites.Molecular microbiology · 2021Article
- Extrachromosomal DNA amplicons in antimalarial-resistant Plasmodium falciparum.Molecular microbiology · 2021Article
- Strain-specific genome evolution in Trypanosoma cruzi, the agent of Chagas disease.PLoS pathogens · 2021Article
- Article
- NewFrontiers in microbiology · 2020Article
- Rapid antigen diversification through mitotic recombination in the human malaria parasite Plasmodium falciparum.PLoS biology · 2019Article
- Adaptation of Translational Machinery in Malaria Parasites to Accommodate Translation of Poly-Adenosine Stretches Throughout Its Life Cycle.Frontiers in microbiology · 2019Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Antimalarial resistance is a major obstacle in the eradication of the human malaria parasite, Plasmodium falciparum. Genome amplifications, a type of DNA copy number variation (CNV), facilitate overexpression of drug targets and contribute to parasite survival. Long monomeric A/T tracks are found at the breakpoints of many Plasmodium resistance-conferring CNVs. We hypothesize that other proximal sequence features, such as DNA hairpins, act with A/T tracks to trigger CNV formation. By adapting a sequence analysis pipeline to investigate previously reported CNVs, we identified breakpoints in 35 parasite clones with near single base-pair resolution. Using parental genome sequence, we predicted the formation of stable hairpins within close proximity to all future breakpoint locations. Especially stable hairpins were predicted to form near five shared breakpoints, establishing that the initiating event could have occurred at these sites. Further in-depth analyses defined characteristics of these 'trigger sites' across the genome and detected signatures of error-prone repair pathways at the breakpoints. We propose that these two genomic signals form the initial lesion (hairpins) and facilitate microhomology-mediated repair (A/T tracks) that lead to CNV formation across this highly repetitive genome. Targeting these repair pathways in P. falciparum may be used to block adaptation to antimalarial drugs.
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