Savannah L
- Research Program Mentor
PhD candidate at Stanford University
Expertise
Microbiology, immunology, genetics, molecular genetics, cell biology, global health
Bio
Hi! My name is Savannah (she/her/hers), and I am a second year PhD student in Microbiology and Immunology at Stanford University. I research the immune response to malaria during pregnancy, specifically focusing on the intersection of innate and adaptive immunity at the placenta. I graduated from Brown University with a BS in Cell and Molecular Biology in 2021, where I did a variety of research - everything from gene regulation in fruit flies to using Nanopore sequencing to learn about the regional distribution of drug-resistant malaria. Fun fact - I played Division I basketball at Brown! Go Bruno! I would not be where I am today without the phenomenal mentors in my life, and I hope to be just as powerful an advocate for my students and mentees one day. I have extensive teaching and mentoring experience, both formal and informal, and it's extremely personally fulfilling. I know what it's like to struggle in coursework and to not initially understand content (I have ADHD and was diagnosed in college), so my approach to teaching is compassionate, patient, and affirming - everyone can succeed with the right support! Outside of the lab, I love to drink life to the lees! From hiking and biking around the South Bay, to browsing museums and going to concerts in San Francisco, to devouring books and podcasts and documentaries, I'm always learning new things, seeing new sights, and experiencing more life. I'm so excited for you to join me!Project ideas
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