Do stress granules help cancer cells survive stress?
Graduate Research Assistant · Baymiller Lab, Central Connecticut State University · July 2026–present
Stress granules are biomolecular condensates of RNA-binding proteins and mRNA. They
form when a eukaryotic cell faces oxidative stress, heat shock, ER stress, or other
stressors that repress translation, binding ribosome-free mRNA together so it cannot
be translated. Their formation and role in translational control have been studied
extensively, but much less is known about how they affect the overall health of the
cell and its ability to survive and reproduce.
My hypothesis is that stress granule formation promotes cancer cell survival during
chemical stress, by protecting mRNA and reorganizing cellular resources while
translation is repressed. If so, cells that can form stress granules should maintain
greater viability and metabolic activity than cells in which their formation is
inhibited. The comparison distinguishes whether stress granules are a passive part of
the stress response or an active mechanism that promotes survival.
To test this, I:
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Induce stress with arsenite and compare cancer cells that form stress granules with
cells treated with halofuginone, a small molecule that inhibits stress granule
formation.
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Measure metabolic activity in each condition with MTT assays.
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Assess cell survival by fluorescence microscopy and quantitative image analysis.
This project is in progress.
A high-throughput assay for proton permeability of lipid membranes
Independent Researcher · Maurer Lab, Central Connecticut State University · Aug 2025–May 2026
Membranes hold the proton gradients that power ATP synthesis, so their proton
permeability matters for modern cells and for the first cells alike. Standard
pyranine-based assays are slow and low-throughput. I built a 96-well plate-reader
version: the pH-sensitive dye pyranine is encapsulated in DOPC vesicles, acid is
added by automated dispenser, and the drop in fluorescence gives a real-time,
quantitative measure of protons crossing the membrane.
I identified and resolved three problems in the method:
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Vesicle quality. Sonication alone often produced oil droplets
instead of bilayer vesicles. Extruding through a 1 µm filter and removing
free dye by size-exclusion chromatography gave small, uniform vesicles, which I
confirmed by fluorescence microscopy.
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Instrument drift. Fluorescence in dye-only controls crept upward
over time. I traced this to the instrument and eliminated it by warming the plate
reader for over an hour instead of the recommended 20 minutes.
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Acid concentration. At low acid concentrations, fluorescence fell
and then rose again. At the highest, it fell too fast to resolve. I found a working
range where the kinetics fit a two-phase exponential model (R² ≥ 0.994
across three replicates), and nigericin controls confirmed that the vesicles held a
proton gradient.
The result is a working 96-well assay with consistent controls, designed to compare
prebiotically relevant amphiphiles and phospholipid membranes exposed to PFAS. Data
from this project was used as the basis for a research grant for the Maurer lab.