Date of Graduation

Spring 2026

Degree

Master of Science in Biology

Department

Biology

Committee Chair

Kyoungtae Kim

Abstract

Quantum Dots (QDs) are nanoparticles that are highly desirable for biomedical applications such as drug delivery, cellular tracking, and imaging due to their fluorescent and tunable optical properties. The toxicity of QDs, however, has raised concerns about their mass adoption. While recent studies have shown QDs’ ability to directly interact with globular actin (G-actin), its impact on actin dynamics and and its regulators, such as α-actinin, have not been explored. Therefore, my thesis focused on the adverse effects of CdSe/ZnS QDs on actin dynamics and α-actinin function and assessed their overall impact on actin cytoskeletal organization. I found that QDs act in a biphasic manner where lower concentrations of QDs stimulate the polymerization of actin, while high concentrations of QDs inhibit it. QDs can also bind to filamentous actin (F-actin) and cause bundling of the filament while also promoting actin depolymerization. QD–α-actinin interactions demonstrated strong binding between QDs and α-actinin, which impeded α-actinin mediated F-actin bundling, as well as compromised the activity of α-actinin from preventing actin depolymerization. Furthermore, the physics-based modeling and simulations carried out in physiological temperature supported these findings by identifying stable interaction surfaces between QDs and α-actinin. Through this study, I proposed a novel mechanism in which QDs negatively influence cellular processes. Finally, my study also provided mechanistic insight into nanoparticle-protein interactions and highlighted the potential cytoskeletal toxicity associated with it.

Keywords

quantum dots, actin dynamics, cytoskeleton, α-actinin, modeling, nanoparticle- protein interactions, cytoskeletal toxicity

Subject Categories

Biology | Molecular Biology | Nanotechnology | Toxicology

Copyright

© Abhishu Chand

Available for download on Saturday, May 08, 2027

Open Access

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