Fly into the Genetic Maze: Unraveling DNA stability and Mutagen
Location
Poster #27
Department
Biology
Abstract
DNA, the fundamental molecule encoding genetic information, undergoes continuous replication and repair processes crucial for the survival and reproduction of living organisms. Mutations, alterations in the DNA sequence, can arise from various factors such as errors during DNA replication, exposure to mutagens, or underlying health conditions. DNA2, an essential gene involved in preserving DNA stability and regulating replication, plays a crucial role in maintaining cellular health. To understand the function of the DNA2 repair gene, we utilized Drosophila melanogaster, commonly known as the fruit fly, as a model organism. With approximately 70% genetic similarity to human disease causing genes, fruit flies have been important in scientific research for decades, serving as a valuable model for studying various diseases. In this study, we investigated DNA2 function in fruit flies using three distinct alleles: DNA2D1, DNA2D2, and DNA2lS. Our goal was to subject DNA2-deficient flies to mutagens that cause different kinds of DNA damage to better understand the contribution of DNA2 to DNA repair. Previously, our lab found that both DNA2D1 and DNA2D2 flies exhibit sensitivity to MMS, which causes large DNA adducts, as well as to mutagens that impair DNA replication. We extended this research by investigating how lower doses of MMS influence the sensitivity of DNA2 mutant flies, as well examining the response of DNA2 mutants to the mutagens bleomycin (double strand breaks) and potassium bromate (oxidative stress). We exposed DNA2lS/D1 and DNA2lS/D2 larvae to mutagens and then calculated relative survival by comparing the percentage of mutagen-treated mutants treated to the percentage of mutants that were untreated. Our results revealed that DNA2lS/D1 and DNA2lS/D2 flies showed similar dose-dependent sensitivity to MMS, suggesting that there is no difference in DNA damage response between the two alleles. DNA2 mutants were not sensitive to bleomycin or potassium bromate. Our results support the previous findings that DNA2 plays a role in responding to replication stress, but is not required in other types of DNA repair. These findings advance our understanding of DNA repair mechanisms, which can lead to future cancer and disease treatments.
Faculty Sponsor
Elyse Bolterstein
Fly into the Genetic Maze: Unraveling DNA stability and Mutagen
Poster #27
DNA, the fundamental molecule encoding genetic information, undergoes continuous replication and repair processes crucial for the survival and reproduction of living organisms. Mutations, alterations in the DNA sequence, can arise from various factors such as errors during DNA replication, exposure to mutagens, or underlying health conditions. DNA2, an essential gene involved in preserving DNA stability and regulating replication, plays a crucial role in maintaining cellular health. To understand the function of the DNA2 repair gene, we utilized Drosophila melanogaster, commonly known as the fruit fly, as a model organism. With approximately 70% genetic similarity to human disease causing genes, fruit flies have been important in scientific research for decades, serving as a valuable model for studying various diseases. In this study, we investigated DNA2 function in fruit flies using three distinct alleles: DNA2D1, DNA2D2, and DNA2lS. Our goal was to subject DNA2-deficient flies to mutagens that cause different kinds of DNA damage to better understand the contribution of DNA2 to DNA repair. Previously, our lab found that both DNA2D1 and DNA2D2 flies exhibit sensitivity to MMS, which causes large DNA adducts, as well as to mutagens that impair DNA replication. We extended this research by investigating how lower doses of MMS influence the sensitivity of DNA2 mutant flies, as well examining the response of DNA2 mutants to the mutagens bleomycin (double strand breaks) and potassium bromate (oxidative stress). We exposed DNA2lS/D1 and DNA2lS/D2 larvae to mutagens and then calculated relative survival by comparing the percentage of mutagen-treated mutants treated to the percentage of mutants that were untreated. Our results revealed that DNA2lS/D1 and DNA2lS/D2 flies showed similar dose-dependent sensitivity to MMS, suggesting that there is no difference in DNA damage response between the two alleles. DNA2 mutants were not sensitive to bleomycin or potassium bromate. Our results support the previous findings that DNA2 plays a role in responding to replication stress, but is not required in other types of DNA repair. These findings advance our understanding of DNA repair mechanisms, which can lead to future cancer and disease treatments.