Jennifer Small-Saunders
Columbia University, NY·Microbiology & Immunology·Early-career
Malaria, caused by the mosquito-borne parasite Plasmodium falciparum, still causes roughly 200 million cases and 600,000 deaths each year, mostly in children under five. The frontline drug artemisinin is losing effectiveness: resistant parasites spread across Asia and have now appeared in Africa.
- Fields
Microbiology & Immunology
Genetics
Biochemistry
- Topics
malaria
Plasmodium falciparum
artemisinin resistance
- Grants
- 1 known grant, through Aug 2027
What they work on
- Identify long noncoding RNAs and tRNA-derived fragments that change in artemisinin-resistant versus sensitive Plasmodium falciparum after drug exposure or isoleucine starvation, using transcriptomics.
- Validate candidate noncoding RNAs as drivers of quiescence using CRISPR/Cas9 conditional knockdowns, which switch genes off on demand, together with in vitro parasite drug susceptibility assays.
- Map molecular mechanisms by using biotinylated candidate noncoding RNAs as bait to capture interacting RNA-binding proteins, identified by mass spectrometry.
- Test whether chemical modifications on amino-acylated tRNA, the carriers that deliver amino acids during protein synthesis, regulate artemisinin-induced dormancy, using specialized mass spectrometry and genetic knockdowns.
- Create a quiescence reporter parasite line enabling live sorting of dormant parasites and single-cell transcriptomic profiling as they enter and exit the dormant state.
More about the research
Resistance is driven mainly by mutations in a parasite protein called K13, and part of how resistant parasites survive is by entering quiescence, a dormant, non-growing state. Only a small but reproducible fraction of parasites survives a drug pulse this way and then restarts growth. What makes a parasite enter dormancy, and what wakes it up, is unknown.
Why it matters
Artemisinin resistance threatens malaria treatment and control worldwide, especially for young children in Africa. Identifying the molecules that let resistant Plasmodium falciparum go dormant and survive a drug pulse could expose parasite vulnerabilities and inform new antimalarial strategies aimed at blocking dormancy or preventing recovery after treatment.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Anthony Ruberto
Florida State University, FL·Microbiology & Immunology·Early-career
Determine the genetic changes underlying the cellular and transcriptomic differences between artemisinin-resistant and -sensitive Plasmodium falciparum, using long-read and short-read sequencing plus Chromosome Conformation Capture sequencing to map genome folding.
Jonathan Juliano
University of North Carolina at Chapel Hill, NC·Microbiology & Immunology·Early-career
Build a temporal deep learning surrogate, a neural network trained on simulation output, to predict how antimalarial drug policy changes would alter resistance and transmission in Kinshasa Province, Democratic Republic of the Congo.
Joshua T Mendell
University of Texas Southwestern Medical Center, TX·Biochemistry
Determine how altering dihydrouridine synthase (DUS) activity changes D modifications on tRNAs, overall tRNA metabolism and the PTMD mRNA-decay pathway in human and mouse ccRCC cells.
The school
Columbia University: 89 labs on PI Pages, $1.4B a year on research, 625 research doctorates a year.
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