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Master of Science (MS) in Biology




Mutation rates vary within and among species, in part reflecting the variable input of the two main sources of mutation, DNA replication errors and DNA damage. In somatic tissues, oxidative damage resulting from free radical attacks on DNA is an important and well-characterized cause of mutation, contributing to many diseases and to the aging process. In contrast, it is not known whether oxidative damage can lead to heritable mutations in germline (sperm and egg) DNA. In a previous study, the germline mutation rate was estimated from a mutation accumulation study in two strains of rhabditid nematode (Caenorhabditis elegans), the N2 strain which has a ‘normal’ free radical metabolism and the mev-1 strain which has constitutively high oxidative stress. Opposite to the predicted results, that study did not detect any differences in mutation rate between the two strains when fitness, the proxy for mutation rate, was measured in a benign (standard laboratory) environment. In the current study, I measured the fitness of a subset of nematodes from the earlier work in two environments, a benign environment (20°C) and a stressful environment (25°C). This comparison across environments allowed me to determine whether the mutation rate or average mutation effect size differed between the two strains. I predicted that the mev-1 nematodes would have a higher overall estimated mutation rate due to their high oxidative stress. Since mutation rate and mutation effect size are inversely related, I predicted that the mev-1 nematodes would have a low estimated effect size in comparison to the N2 nematodes. I measured reproductive fitness in the two strains of nematodes by conducting a fitness assay in two environments, a stressful and a benign environment. The mev-1 nematodes had a low average genomic mutation rate and a large average estimated effect size when compared in two environments. This results was opposite to my predictions. A possible interpretation is that the mev-1 strain did not accumulate more mutations (low mutation rate) and/or that the mev-1 nematodes could not tolerate the mutations they accumulated, especially in the stressful environment (high average effect size). Many organisms upregulate cellular protection against chronic stress. It would be of interest to investigate if the mev-1strain upregulate repair and/or protective proteins. Overall, I did not find evidence that the widespread consequences of oxidative stress that are documented in somatic tissues are occuring in the germline. This study did not provide evidence that conditions that elevate oxidative stress in the germ cells (sperm and eggs), including age and environmental exposure, impact the quality of germline DNA.

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