Bin Gu is an assistant professor in the Department of Obstetrics, Gynecology and Reproductive Sciences. He joined MSU from the Hospital for Sick Children, Toronto, Canada, where he developed new genome editing technology to engineer mouse models and study embryonic development and human genetic diseases. Dr. Gu obtained his B.S. in Biotechnology and Ph.D. in Cell Biology at the Zhejiang University, China. He then worked at the Hospital for Sick Children as a postdoc in 2013, where he made seminal contributions to the genome editing technologies for building complex mouse genetics models and our understanding of early embryo development.
The Gu Lab
The research in Gu Lab focuses on investigating the genetic mechanisms of fertility defects and genetic disease. We model human disease state by building mouse models recapitulating human complex mutations. We study normal and defective developmental process in real-time by building and live imaging reporter mouse models. We leverage state of the art genomics and stem cell technologies to dissect the molecular mechanisms of genetic diseases. The knowledge gained in our research will allow us to better understand the genetic basis of human fertility defects and congenital diseases and to develop new therapeutic strategies such as gene therapy.
Micro-injecting CRISPR-Cas9 reagents into 2-cell stage mouse embryos allow efficient genome editing by 2-cell-homologous recombination(HR)-CRISPR (Nature Biotechnology 2018).
Mouse blastocysts are ideal models to study pre-implantation development and fertility defects rooted in preimplantation stages. By live imaging this blastocyst in which all three lineages are marked by specific reporters, we can understand normal and defective pre-implantation development in real-time.
Large genomic duplication or translocations underlies a broad spectrum of human genetic diseases. We developed new genome editing technologies to generate mouse models carrying these types of complex mutations. The Mecp2 duplication model that we built recapitulates the genomic duplication in human patients and offers a crucial model for developing gene therapies.
Contact
