Eukaryotic cells use a variety of mechanisms to protect themselves from the harmful effects of DNA damage. DNA repair enzymes recognise and remove damage, checkpoint control pathways delay cell division while repair occurs, and in some cases cell death or apoptosis is activated to ensure that damaged cells are removed from organisms. 

Defects in DNA-damage responses lead to diseases associated with ageing and cancer.  For example, Werner's syndrome, a genetic disease associated with premature human ageing, is associated with a mutation in a gene encoding a DNA repair protein.  In cancer, more than half of all human tumours contain mutations in the p53 checkpoint protein.

Our lab uses genetic, systematic, molecular and biochemical approaches to understand the interplay between DNA damage responses and telomeres in the model organism Saccharomyces cerevisiae (budding yeast).  The telomere is the DNA-protein complex at the end of eukaryotic chromosomes that caps the ends of chromosomes to stop the ends being recognised by DNA repair and checkpoint complexes. 

By conditionally inactivating telomere capping proteins in yeast we can monitor the effects of DNA repair and checkpoint genes at telomeres.  Since the biochemical mechanisms underlying DNA-damage responses are largely conserved between yeast and human cells our studies in a simple, yet powerful model system, are of direct relevance to human health.