DNA Repair, Gene Editing & Gene Therapy

Our lab revealed the mechanism of APOBEC cytidine deaminase-mediated mutagenesis during the repair of CRISPR/Cas9-generated DNA breaks. We developed multiple series of base editors, including enhanced base editors (eBEs) with improved product purity and editing efficiency, dCpf1 base editors (dCpf1-BEs) for editing in A/T-rich regions, human APOBEC3A base editors (hA3A-BEs) for efficient editing in G/C-rich and/or highly methylated regions, dCas12a-hA3A base editors (BEACON) for efficient editing with only background levels of DNA damage response and transformer base editors (tBEs) for eliminating gRNA-dependent and gRNA-independent off-target mutations. We also determined the genome-wide and transcriptome-wide off-target effects by prime editor 3 (PE3) and developed sPE and aPE systems with improved editing efficiency.

Our lab focuses on DNA repair-induced mutagenesis, the development and application of new gene editing systems and gene editing therapy. We are particularly interested in: (1) DNA repair-induced mutagenesis in gene editing, carcinogenesis and aging; (2) Development of new gene editing tools; (3) Gene editing therapy for human disease.