Jennifer Guler
University of Virginia, VA·Microbiology & Immunology·Early-career
Single-celled organisms can adapt quickly when they face drugs, heat or nutrient shortages. One way is by changing their DNA.
- Fields
Microbiology & Immunology
Genetics
Biology
- Topics
malaria
Plasmodium falciparum
apicomplexa
- Grants
- 3 known grants, through Jul 2027
What they work on
- Test whether the extreme AT content of the Plasmodium falciparum genome drives DNA breaks and copy number variations by comparing human-infecting malaria species with different AT levels, using highly accurate genome assemblies.
- Measure how often new copy number variations arise in Plasmodium under normal and stressed conditions, and identify genome features linked to DNA breakage in vivo.
- Trace the lifecycle of circular extrachromosomal DNA in Plasmodium, including its ties to chromosomal genes and its diversity, using microscopy, molecular genomics and computation.
- Identify the cellular pathways and sequences that generate and stabilize ecDNA, and map how ecDNA clusters within the parasite nucleus.
- Characterize how Plasmodium, which lacks the mTOR nutrient-sensing kinase, responds to heat and nutrient stress, using multi-omics data and computational cross-species comparisons.
- Generate open-access multi-omics datasets and mutant parasite lines to reveal which parts of the early-branching eukaryote stress response differ from those of higher organisms.
More about the research
The malaria parasite Plasmodium is an especially useful system for studying this process. It grows easily in the lab, has an unusual genome extremely rich in the DNA bases A and T, and adapts rapidly, for example by becoming drug resistant. The lab's projects ask how genome features and cellular responses let these parasites adapt. They cover three linked questions: how stretches of DNA get copied, how DNA circles form outside the chromosomes, and how cells sense and survive stress.
Why it matters
Malaria parasites become drug resistant partly through DNA duplications and extra DNA circles. Learning how these form could help researchers limit this kind of adaptation in microbes, and possibly in fast-evolving cells such as cancers. The work could inform efforts against antimicrobial resistance and cancer progression. Data and mutant parasite lines will also be shared openly.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
The generation, maintenance, and function of extrachromosomal DNA in a divergent eukaryote
NSF · Aug 2024 – Jul 2027
The evolution of copy number variations in the AT-rich Plasmodium genome
NIH · Apr 2021 – Mar 2027
CAREER: A paired experimental-computational approach to elucidate stress responses in early-branching eukaryotes
NSF · Jan 2021 – Dec 2026
Closest labs
Juan Lucas Argueso
Colorado State University-Fort Collins, CO·Genetics
Measure rates of copy number variation (CNV), loss of heterozygosity (LOH), and whole-chromosome gain or loss in dividing and meiotic budding yeast cells, using custom, highly sensitive cell-based assays.
Marjorie Matocq
University of Nevada-Reno, NV·Ecology & Evolution
Identify individual copy number variation (CNV), differences in how many copies each animal carries, in detoxification genes across a woodrat hybrid zone between Neotoma fuscipes and N. macrotis, using genome sequencing.
The school
University of Virginia: 43 labs on PI Pages, $814M a year on research, 413 research doctorates a year.
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