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Distinguishing double-strand DNA breaks from telomeres

Jonathan Strecker

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Canadian Institutes of Health Research (CIHR)
Cancer affects the lives of many Canadians and can arise due to adverse changes in a cell's DNA. The goal of my work is to understand how cells protect their DNA from these changes and what happens when they are no longer able to do so. Our DNA is divided into numerous chromosomes which are linear strands and contain two ends called telomeres. When damaged these DNA strands can also break into pieces which pose a problem to the cell as they need to be accurately put back together. To do this, cells must be able to distinguish ends generated by the break from the natural telomeric ends of the chromosome. The goal of my research is to understand how cells make this distinction. When an end of DNA is found, how does the cell know if it is a break which needs to be repaired, or if it is a telomere which needs to be protected from repair and instead elongated with telomerase? To do this I use the simple model organism budding yeast to study how different DNA ends are dealt with by the cell. I am investigating a key protein in this process, Pif1, which acts at DNA breaks and inhibits telomerase. Interestingly, once DNA ends begin to resemble telomeres, Pif1 is no longer active. My project will characterize and investigate the mechanism of this observation with the hope of identifying similar mechanisms in human cells. This work will help our understanding of a key chromosome biology question and reveal how cells normally prevent certain errors which can lead to cancer.

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