Michael T. Ferdig

The paper functionally validates the Plasmodium falciparum K13 C580Y mutation in Ethiopian isolates, showing it confers artemisinin tolerance.

The paper investigates the bimodal piperaquine response in Plasmodium falciparum by analyzing metabolic, transcriptional, and molecular dynamics data to identify the role of plasmepsin II/III copy number and pfcrt mutations.

This paper develops and validates a qPCR-based assay to measure growth, resistance, and recovery of Plasmodium falciparum after artemisinin treatment, showing distinct phenotypes with independent genetic determinants.

The paper investigates the fitness consequences of selfing and outcrossing in malaria parasites using fluorescent-labelled clones and finds an outcrossing advantage linked to faster sporozoite maturation and increased recombination.

The paper evaluates the impact of K13 mutations on artemisinin resistance and parasite fitness in Bangladeshi Plasmodium falciparum isolates, finding that R561H confers extreme resistance and fitness advantages.

MalKinID identifies malaria parasite genealogical relationships using IBD proportions and segment distributions, showing high accuracy in outcrossed importations but reduced performance in inbreeding scenarios.

This paper evaluates multiple gene co-expression network inference methods for Plasmodium falciparum to improve functional annotation of its genes.

This study uses a genetic cross of Plasmodium falciparum isolates to analyze the roles of pfcrt and pm2/3 in piperaquine resistance and fitness traits.

This study identifies pfaat1 as a key gene in chloroquine resistance evolution in malaria parasites, showing it modulates resistance and fitness through amino acid transport.

This study optimizes bulk segregant analysis for identifying drug resistance loci in Plasmodium falciparum using genetic crosses in humanized mice, confirming the kelch13 locus and demonstrating the utility of cryopreserved pools.

This paper introduces cyclical regression covariates to remove confounding from developmental gene expression in Plasmodium falciparum, improving drug response analysis in clinical samples.

The paper identifies genes in Plasmodium falciparum that enable survival at febrile temperatures and links these to artemisinin resistance through apicoplast-related pathways.

The paper uses bulk segregant analysis to identify genetic loci affecting malaria parasite growth in different media, finding EBA-140 as a key gene involved in media-dependent fitness.

The paper reports two new genetic crosses of Plasmodium falciparum in humanized mice, showing significant variation in marker segregation and demonstrating improved power for genetic mapping of malaria traits.