January 19^th, 2024 – 2:00 to 3:00pm
224 Weill Hall

Yutong Zhu, Yu Lab “Characterization of Human Enhancer Architecture with STARR-seq Based Assays”

 Abstract: Promoters and enhancers serve as pivotal control hubs in gene regulation. Recent studies have unveiled a fascinating parallel between promoters and enhancers, showcasing the presence of divergent transcription events in both. While the TATA box and downstream core promoter regions (DPR) are well-established motifs in promoters, their presence and functional significance in enhancers remain relatively unexplored. Leveraging STARR-seq assays, which are inherently self-transcribing, allows us to investigate enhancer activity through lens of transcriptional signals. Our preliminary results indicate that, for enhancers, it is not only the core promoter regions but also sequences extending up to polymerase pause sites that are crucial for the manifestation of full regulatory activities. This analysis of enhancer boundaries holds significant implications, as it can determine whether the location of a GWAS hit near an enhancer could potentially impact gene expression.

Yu Sun, Yu Lab “Brain Cell-Specific Protein Interactome Mapping Interprets Genetic Signals in Alzheimer’s Disease”

Abstract: Alzheimer’s disease (AD), a progressive disease that affects memory and other important mental functions, has been identified relevant to more than 75 genetic variants associated with in recent Genome-wide association studies (GWAS). However, translating those nominated genetic findings to the functional interpretation in different brain regions remains elusive. Besides, brain cell-specific protein interactome data is limited for AD. In this project, we will utilize high-throughput Immunoprecipitation-Mass Spectrometry (IP-MS) for 87 AD risk genes that have been identified by recent GWAS studies and public datasets to generate brain cell-type-specific interactome mapping. Our current results not only overlapped with high-profile interactome data, such as OpenCell and BioPlex, but also identified novel interactions that are relevant to AD pathology. Meanwhile, such complementary interactome mapping will provide an organized framework to facilitate interpretations of genetic and transcriptomic data in AD and other related neurodegenerative diseases.