SEMINAR: Bayliss Seminar Series

Alternative splicing plays a pivotal role in normal development and key cellular processes via its capacity to promote diversity in mRNA and protein isoforms. Aberrant alternative splicing has been found in many disease states including cancer. Therefore, understanding the mechanisms underlying alternative splicing has remained an important area of research. Emerging evidence has indicated a crucial role of epigenetic and chromatin structure in regulating alternative splicing. DNA methylation is one of the most important epigenetic modifications and its role in regulating gene expression has been well established, yet the role DNA methylation in regulating alternative splicing has been just evolving.

DNA methylation has been shown to associate with alternative splicing, however, the mechanism of how DNA methylation regulates alternative splicing and whether or not it plays a causative role in splicing regulation is not well understood. Recent advances in precision epigenome engineering with the capacity to mediate site-specific modifications in the epigenome landscape have provided us the unprecedented opportunity to explore the causative role of DNA methylation in splicing regulation.

My PhD research aims to apply the cutting edge epigenome editing tools to modify specific DNA methylation correlated with splicing in two different models, the human B cell lymphoma and the human breast cancer cell models, to investigate the mechanism of DNA methylation in alternative splicing regulation. Successful outcome of the projects might also expand the current method of modulating aberrant alternative splicing in diseases such as cancer by altering specifically the associated DNA methylation marks.