BIO

My name is James Cohan and I am a first-year student at Florida State. I have loved scientific research for many years, and my interests range from the biomedical sciences to molecular biology. My favorite aspects of research are the time spent in the lab and the amount of critical analysis of complex topics. My dream is to combine my love of research with my passion for medicine in an MD/PhD program. This way I can continue with research while practicing clinical medicine and directly making a positive impact on people's lives.

Investigating the Role of a Schizophrenia Risk Gene in Protein Degradation

Abstract

The 14-3-3 protein family is genetically linked to schizophrenia, and studies found that mouse models with 14-3-3 deficiencies exhibit schizophrenia-like behaviors and anatomical abnormalities, including a reduction in dendritic spine density in the brain. Dendritic spines are small protrusions that comprise the postsynaptic compartment of excitatory synapses in the central nervous system. Numerous signaling pathways regulate the actin cytoskeleton of dendritic spines to mediate their proper formation and maintenance. Previous studies identified δ-catenin, an adhesive junction-associated protein crucial in the modulation of actin dynamics, as a potential binding target of 14-3-3. Due to this correlation, 14-3-3 proteins have been studied for their interactions with δ-catenin, although there is conflicting data on how they affect one another. We set out to determine the exact relationship between 14-3-3 and δ-catenin by expressing δ-catenin in a heterologous system for 24 hours and examining remaining δ-catenin levels at several time intervals after overexpression or inhibition of 14-3-3 proteins in vitro. Our preliminary results suggest that 14-3-3 overexpression stabilizes δ-catenin, while the effect of 14-3-3 inhibition remains to be determined. This indicates that 14-3-3 proteins may play a role in the formation of dendritic spines by supporting δ-catenin stabilization in an undetermined pathway.

Keywords: Schizophrenia & protein degradation