Description:

Billions of base pairs of DNA must be replicated trillions of times during a human lifetime. Adding to the difficulty, thousands of DNA lesions happen in each cell of our body every day. Furthermore, replication is challenged by difficult to replicate sequences and conflicts with transcription. To combat these threats, DNA damage response mechanisms act to repair the damaged DNA, signal cell cycle checkpoint activation, ensure completion of DNA replication, and maintain genome stability. Defects in these mechanisms cause developmental abnormalities, premature aging, and cancer. We have utilized a proteomic approach invented by a former graduate student called iPOND to inventory and track ~600 proteins that act at active and damaged replication forks. This approach identified proteins including ETAA1, RADX, and HMCES that act in different replication-stress response pathways. I will present our latest discoveries about how these proteins function to maintain genome stability.

David Cortez, PhD
Professor, Department of Biochemistry
Ingram Professor of Cancer Research
Co-Leader, Genome Maintenance Program, Vanderbilt-Ingram Cancer Center
Vanderbilt University School of Medicine