bioRxivEvolutionary Biology
Genetic mapping of fitness determinants across the malaria parasite Plasmodium falciparum life cycle
X. Li, S. Kumar, M. McDew-White, M. Haile, I. H. Cheeseman, S. Emrich, K. Button-Simons, F. Nosten, S. Kappe, M. Ferdig, T. Anderson, A. Vaughan
Abstract
Malaria is transmitted through female Anopheline mosquitoes where gamete fusion and meiosis occurs, and humans where parasites proliferate asexually. We describe a powerful approach to identify the genetic determinants of parasite fitness across both invertebrate and vertebrate life-cycle stages in human malaria parasite Plasmodium falciparum using bulk segregant analysis (BSA). We combined experimental genetic crosses using humanized mice, with selective whole genome amplification and BSA at multiple developmental stages in both mosquito and vertebrate host to examine parasite competition and identify genomic regions under selection. We generated crosses between artemisinin resistant (ART-R, kelch13-C580Y) and ART-sensitive (ART-S, kelch13-WT) parasite clones recently isolated from Southeast Asian patients. We then quantified genome-wide changes in allele frequency in the parasite progeny population from infected midgut and salivary glands of Anopheles stephensi mosquitoes, infected livers, emerging merozoites and aliquots of in vitro cultured progeny parasites at intervals over 30 days. Three striking results emerge: we observed (i) a strong skew (>80%) towards alleles from the ART-R parent in the mosquito stage, that dropped to [~]50% in the blood stage as selfed ART-R parasites were selected against; (ii) highly repeatable skews in allele frequencies across the genome in blood stage parasites; (iii) particularly strong selection (selection coefficient (s) [≤] 0.18/asexual cycle) against alleles from the ART-R parent at loci on chromosome 12 containing MRP2 and chromosome 14 containing ARPS10. This approach robustly identifies selected loci and has strong potential for identifying parasite genes that interact with the mosquito vector or compensatory loci involved in drug resistance.
- organism: human
- organism: mouse
- assay: bulk RNA-seq
- research focus: variant effect prediction
- approach: statistical model
Reproducibility ledger
Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.
Sign in to file a reproducibility report.
Related papers
- Optimizing bulk segregant analysis of drug resistance using Plasmodium falciparum genetic crosses conducted in humanized mice
Katelyn M. Vendrely, Xue Li, … Tim Anderson·iSciencePeer-reviewed·Mar 16, 2022
- Mapping the genomic landscape of multidrug resistance in Plasmodium falciparum and its impact on parasite fitness
Sachel Mok, Tomas Yeo, … David A. Fidock·Science AdvancesPeer-reviewed·Nov 8, 2023
- Bulk segregant analysis reveals environment x genotype interactions determining malaria parasite growth
Sudhir Kumar, Xue Li, … Tim Anderson·bioRxiv·Sep 12, 2020
- Surprising variation in the outcome of two malaria genetic crosses using humanized mice: implications for genetic mapping and malaria biology
Katrina A. Button-Simons, Sudhir Kumar, … Ian H. Cheeseman·bioRxiv·Dec 13, 2019
- Temporal patterns of haplotypic and allelic diversity reflect the changing selection landscape of the malaria parasite Plasmodium falciparum
Angela M. Early, Stéphane Pelleau, … Daniel E. Neafsey·Molecular Biology and EvolutionPeer-reviewed·Mar 30, 2025
- Xeno-monitoring of molecular drivers of artemisinin and partner drug resistance in P. falciparum populations in malaria vectors across Cameroon
Francis Nongley Nkemngo, Leon M. J. Mugenzi, … Charles Sinclair Wondji·GenePeer-reviewed·Feb 17, 2022