David Lydall

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Our lab uses molecular, genetic and systematic approaches to understand how genetic and chromosomal stability is controlled. 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.  

We are particularly interested in how chromosome ends - telomeres - permit cell division and inhibit DNA repair. The telomere is the DNA-protein complex at the end of eukaryotic chromosomes that stops the ends being recognised by DNA repair and checkpoint complexes.  By conditionally inactivating essential telomere capping proteins in Saccharomyces cerevisiae (budding 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.