Date of Graduation

Spring 2025

Degree

Master of Science in Biomedical Sciences

Department

School of Heath Sciences

Committee Chair

Joshua Smith

Abstract

RecA homologs, Dmc1 and Rad51, work to repair DNA double-strand breaks (DSBs) within the cell through the recombination of homologous sections of DNA. Dmc1 works to repair programmed DSBs through meiotic recombination, while Rad51 functions to repair both meiotic and non-meiotic DSBs, the latter repaired through the process of homologous recombination repair (HHR). Chemotherapeutics, exogenous agents, work to form DSBs in cancer cells, attempting to inhibit the cell’s growth. A hyper recombinant phenotype is often seen in cancer cells due to the overexpression of RAD51, leading to drug resistance, the persistence of cancers, and an overall poor patient outcome. In the model organism Tetrahymena thermophila, an amacronuclear phenotype and increase in cell diameter phenotype is observed at elevated growth temperatures when RAD51 is overexpressed. A complication in elongation of the macronucleus occurs, but DNA synthesis is not halted, resulting in a macronucleus containing up to 5 times the normal genetic content. When DMC1 is overexpressed, an amacronuclear phenotype is observed at a reduced level; though, cell diameter does not increase. Further study between the two RecA homologs will help elucidate how RAD51 overexpression leads to genomic instability in the cell.

Keywords

homologous recombination, DNA double strand break, RecA, Tetrahymena thermophila, macronucleus, amacronucleate, Rad51, Dmc1, meiotic recombination, DNA replication

Subject Categories

Cancer Biology | Genetic Processes | Genetic Structures | Medical Cell Biology | Medical Molecular Biology

Copyright

© Jianna M. Cox

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