Our Core Research Team
We are nine independent laboratories working together to research (i) mechanisms of DNA damage and repair, (ii) translational applications of genome instability to the clinic and (iii) the pathways underlying human cellular aging.
DNA Damage & Repair Researchers
Cellular Aging Researchers
Dr. Tara Beattie
Short Bio Summary
Dr. Tara Beattie is an Associate Professor in the Departments of Biochemistry and Molecular Biology and
Oncology. She obtained her PhD from the University of Toronto in 1997 and completed her post-doctoral
training with Dr. Lea Harrington and the Ontario Cancer Institute from 1997-2000. In 2001, she became an
independent investigator at the University of Calgary in the Cumming School of Medicine.
My lab focuses on telomere integrity and the enzyme telomerase as a critical factor in the progression of age-related diseases. Telomeres are specialized structures that form the protective ends of linear chromosomes. Telomeres confer stability of our DNA and therefore, telomere structure needs to be maintained in cells, since changes in DNA integrity can lead to multiple disease states. Activation of the enzyme telomerase, which maintains telomere length in dividing cells, is essential for the unregulated growth of many cancer cells. However, in addition there are at least four three disease states that arise from mutations in telomerase, stressing the importance of the delicate balance that must be preserved between telomerase activation and telomerase inhibition – either too much, or too little of the enzyme can be bad for the cell.
Since cellular and organismal aging are influenced by numerous factors including telomere length, telomerase activity and the DNA damage response, it will be critical to understand the interplay between each of these processes in healthy aging and how these processes go awry in age-related diseases. We are aiming to understand the interplay between telomere length maintenance, cell growth, the DNA damage response and checkpoint activation to understand how telomere dysfunction/telomerase mutations might contribute to disease states and aging.