Guo Caixia

Biography

Dr. GUO Caixia，Professor at Beijing Institute of Genomics, Chinese Academy of Sciences (CAS) and hundred-talent program of CAS. She received her B.S. degree in cell biology from Wuhan University in 1991 and a Ph.D. degree in physiology from the Institute of Zoology, CAS in 1999. She began her first postdoctoral training in the department of Physiology at the University of Kentucky to study the regulation of estrogen receptor beta expression in the ovary. In 2001, she joined Dr. Errol C. Friedberg's lab in UT Southwestern Medical Center as a postdoc to study the mechanisms of DNA damage tolerance. Later she was promoted to be a faculty member in the department of Pathology at UT Southwestern Medical Center (instructor during 2004-2008 and assistant professor since 2008). She is editorial board member for journal Genomics, Proteomics & Bioinformatics since 2010 and has undertaken many research projects from 973, General Program of National Nature Science Foundation of China etc. Her papers have been published in high quality scientific journals, including Cell、Mol Cell、PNAS、EMBO、NAR、Human Mol Genet etc. She has been focusing on studying the mechanisms of translesion DNA synthesis in vivo. The long term goal of her work is to understand how TLS polymerases contribute to genomic instability and tumorigenesis. A wide spectrum of experimental approaches will be employed, including molecular and cellular biology, biochemistry, genomics and proteomics etc.

Research Interest

The human genome is constantly threatened by a variety of endogenous and environmental factors. Although most of DNA damage can be repaired through multiple DNA repair pathways, some DNA lesions inevitably escape from the surveillance of DNA repair system and lead to replication forks collapse. Cells evolve a translesion DNA synthesis (TLS) mechanism to incorporate nucleotides opposite damaged lesions by using low fidelity DNA polymerases. TLS includes an error-free pathway and an error-prone pathway, and the latter of which is responsible for the most of genome mutations induced by environmental carcinogens and other DNA damage reagents. Therefore it is believed that reducing error-prone TLS might help control carcinogenesis. Unfortunately, it remains elusive how cells regulate TLS in vivo. The current ongoing projects include: 1, the mechanism of TLS regulation after diversity of DNA damage agents treatment; 2, Genome instability caused by environmental toxic reagents/ chemotherapeutic drugs and related human diseases (infertility, cancer and ageing, etc); 3, the role of RNA binding proteins in DNA repair and genome stability.