ELISE KIM

Yanlin Liu

MARSHALL COLLEGE NEUROBIOLOGY & CLINICAL PSYCHOLOGY MAJOR

Signal transducer and activator of transcription 3 (STAT3) is a transcription factor reported to be involved with tumor initiation and progression. Additionally, STAT3 activation is associated with adaptive responses to stress commonly associated with the tumor microenvironment such as oxidative stress, hypoxia, and nutrient deprivation. Similarly, cellular stress have been reported to stimulate tumor progression. To investigate STAT3’s role in response to cellular stress, we engineered STAT3 knock-out (KO) cells using the CRISPR Cas9 system. Here we report the establishment of STAT3-KO clones generated in a pancreatic cancer cell line model. Furthermore, STAT3 depletion and their functional inactivation of STAT3 signaling was validated through western blot analysis. Though STAT3 is widely accepted as an oncogene, STAT3 targets genes involved in its adaptive stress responses remain poorly understood. These STAT3-KO clones will be instrumental for future studies investigating STAT3’s role in cellular stress responses and the identification of its downstream effectors.

REVELLE COLLEGE HUMAN BIOLOGY MAJOR PSYCHOLOGY MINOR

PI: Robert Rissman, Ph.D., UCSD School of Medicine, Department of Neurosciences

PI: Yimin Zou, Ph.D., UCSD School of Biological Sciences, Department of Neurobiology

Abby Lee

PI: Deborah Yelon, Ph.D., UCSD School of Biological Sciences, Department of Cell and Developmental Biology

SIXTH COLLEGE BIOINFORMATICS MAJOR COMPUTER SCIENCE MINOR

Dysregulation of snoRNAs is implicated in cancer and neurological diseases— for example, in amyotrophic lateral sclerosis (ALS), a mutation in FUS dysregulates a subset of snoRNAs responsible for ribosomal RNA modification, hampering translation efficiency. To systematically study snoRNA biogenesis and function, I aim to build a framework that utilizes >200 publicly available enhanced crosslinking and immunoprecipitation (eCLIP) datasets to probe RBP binding sites on snoRNAs and identify potential snoRNPs using clustering analysis. To understand the mechanisms by which a RBP mutation leads to the dysregulation of a subset of snoRNAs, I identify RBPs and protein-complexes with enriched binding sites on these dysregulated snoRNAs. With this computational framework, we are able to better understand the biogenesis and function of snoRNAs.