Michael Soniat, PhD

My laboratory is primarily interested in understanding how molecular machines maintain genome integrity. We use a combination of innovative techniques encompassing a broad range of disciplines, from single-molecule biophysics and structural biology to biochemistry and cell biology, to determine the mechanisms by which macromolecular complexes function to prevent genome instability at the molecular level, providing insights into how they prevent accelerated aging and cancer. Projects in the lab include determining the molecular mechanisms underlying telomere length regulation. Telomere length regulation is vital for maintaining cellular homeostasis and requires a balance between lengthening and shortening processes. Critically short telomeres can lead to genome instability, cellular senescence, or apoptosis which are critical drivers in cancer development and several aging disorders. Furthermore, excessively long telomeres have also been shown to increase cancer risk. Therefore, we are interested in answering critical questions regarding telomeric maintenance by directly observing the dynamic assembly of large multi-protein complexes on telomeric DNA, which are necessary to control telomere length and protect telomeric integrity. We are also interested in understanding how cells repair damaged DNA beyond telomeres and along chromatin. In particular, we are interested in deciphering how DNA repair proteins locate, assemble, and are regulated at DNA double-strand breaks to promote error-free repair and prevent genome rearrangements and malignant transformation. Ultimately, our long-term goal is to increase our understanding of how genome instability contributes to cancer and aging and to aid in developing new strategies to delay age-related diseases.

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