Dr. Katheryn Meek

Biography

Research focuses on the mechanisms by which DNA, the blueprint of living organisms, is maintained and repaired. The evolution of organisms has led to the development of numerous strategies to ensure the accurate copying of genomes for propagation. Despite the critical role DNA plays in life, it is surprisingly sensitive to various forms of damage, including oxidation, hydrolysis, and methylation. Laboratory studies concentrate on DNA double strand breaks (DSBs) and the major repair pathways involved, including non-homologous end joining (NHEJ) and homologous recombination (HR). NHEJ, the primary repair mechanism in higher eukaryotes, is actively engaged during the cell cycle, particularly when the sister chromatid is available as a repair template in the S and G2 phases. Emerging research indicates the existence of additional repair pathways that contribute to the resolution of DSBs, especially in the absence of NHEJ, although the exact composition and roles of these pathways remain to be fully understood. The laboratory specifically studies the large serine/threonine protein kinase known as DNA-dependent protein kinase (DNA-PK), which initiates NHEJ by recognizing DNA ends and targeting NHEJ factors to the site of damage. Recent data suggest DNA-PK is a central regulator of DNA end access, with ongoing studies aiming to elucidate how DNA-PK regulates this access, primarily through autophosphorylation to promote end joining with minimal sequence information loss. Additionally, it has become evident that DNA-PK influences repair pathways, potentially limiting the accessibility of DNA ends to repair factors, which may be particularly significant in species that express high levels of DNA-PK, thus partially elucidating the varying roles DNA-PK plays across different species.

Research Interests