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Savannah

PhD Doctor of Philosophy candidate

Expertise
Microbiology, immunology, genetics, molecular genetics, cell biology, global health

Project ideas

Project ideas are meant to help inspire student thinking about their own project. Students are in the driver seat of their research and are free to use any or none of the ideas shared by their mentors.

Seeking single (X) males: dosage compensation and X-identification in Drosophila

Understanding the mechanisms of dosage compensation in a model system, such as Drosophila melanogaster, can help scientists better understand human genetic diseases. Dosage compensation is the process by which organisms equalize the expression of genes between the different biological sexes. Two key regulators of this process in Drosophila are Male Specific Lethal Complex (MSL), which increases transcriptional output of a male’s single X-chromosome to equal XX females, and Chromatin-Linked Adapter for MSL Proteins (CLAMP), which binds genome-wide, but recruits MSL only to the X-chromosome. Although CLAMP’s binding motifs are GA-rich, it is not well-understood how CLAMP is able to distinguish an X-chromosome from an autosome, and thus consequently recruit MSL.

Hijacking the host: malarial manipulation of human host kinases

The malaria parasite provides researchers with an opportunity to characterize invasion and pathogenesis strategies that have been refined throughout evolutionary history. Malaria is the disease caused by unicellular eukaryotic parasites in the Plasmodium genus, and it remains one of the largest global health challenges despite decades of international control efforts. Several studies have demonstrated that well-characterized human signal transduction molecules (ex: G-coupled protein receptors, MAP/ERK kinase, p21-activated kinase, protein kinase C, peroxiredoxin) are necessary for parasite proliferation. Pharmacological interference with the function of said molecules results in parasite death comparable to frontline antimalarial drugs in vitro. A recent comprehensive analysis revealed that malaria-infected erythrocytes have a significantly higher proportion of phosphorylated signaling molecules than uninfected erythrocytes. Phosphorylation patterns are also life cycle stage-specific, strongly suggesting the parasite manipulates host factors to support its survival. It has yet to be demonstrated that malaria is biochemically capable of phosphorylating erythrocyte signaling proteins, and whether or not these phosphorylated proteins alter intracellular cellular conditions in a way that directly benefits the parasite remains to be determined

Coding skills

R, command line

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