The mechanisms by which APOBEC3 cytidine deaminases promote genomic instability

Dr Linda Chelico
Professor and Department Head
Microbiology, and Immunology
College of Medicine, University of Saskatchewan, Canada

This special conference is hosted by Javier Di Noia. 

About this conference
APOBEC3A and APOBEC3B are deoxycytidine deaminases that induce somatic mutations that are prevalent in cancers. In addition, these APOBEC3s can efficiently displace RPA to access ssDNA, suggesting that they may also affect downstream DNA repair processes. To investigate this possibility, we used mass spectrometry-based analyses of APOBEC3-protein interactions in cells and proteins accumulating at replication forks in the presence of an APOBEC3. The data support that APOBEC3A displaces telomerase and DNA repair proteins from DNA and that APOBEC3B is associated with higher cMyc levels in cells. These activities enable APOBEC3A and APOBEC3B to promote genomic instability beyond the well characterized deoxycytidine deaminase activity.

About Linda Chelico
Dr. Linda Chelico is a Professor and Head of the Department of Biochemistry, Microbiology, and Immunology at the University of Saskatchewan. Her research focuses on the APOBEC3 family of cytidine deaminases, enzymes that protect the human body by restricting viral replication, such as HIV-1, but can also introduce mutations that contribute to cancer development. Using biochemical and cellular approaches, her laboratory investigates how APOBEC3 enzymes interact with viral proteins like HIV-1 Vif, and how their activity impacts genomic integrity and tumorigenesis.

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