| Description |
DNA is the blueprint of all biological life as it provides the means necessary for sharing of genetic information. DNA is formed and stabilized by interactions between four unique bases, Adenine (A), Cytosine (C), Guanine (G), and Thymine (T) which come together in predetermined patterns to create a two-stranded structure known as the double helix. Genetic information is stored in the precise pairing and arrangements of the four bases, encoded in the form of a sequence to allow correct information to be sent to replicated strands. Adenine must pair with Thymine, and Guanine must pair with Cytosine to retain the stability and information of the DNA. However, exposure of DNA to reactive oxygen and nitrogen species (ROS) lead to chemical damage, DNA base modifications, and incorrect pairings of bases. This mispairing caused by DNA damage can ultimately result in mutations, permanent changes to the information encoded in the DNA sequence, which can lead to malignant cellular phenotypes and life-threatening diseases such as cancer (Banda et al. 2017). For billions of years, biological systems have been exposed to DNA damage, creating selective pressure that resulted in an ensemble of DNA repair strategies through evolution. My Honors Thesis focuses on the base excision DNA repair enzyme MutY in bacteria and its homologous protein in humans, MUTYH. MutY and MUTYH prevent the accumulation of mutation in DNA by working with partner proteins belonging to the GO DNA repair pathway. |
