Honors Theses and Capstones

Date of Award

Spring 2014

Project Type

Senior Honors Thesis

College or School



Molecular, Cellular and Biomedical Sciences

Program or Major


Degree Name

Bachelor of Science

First Advisor

Vaughn S. Cooper

Second Advisor

Marcus M. Dillon


Mutations are the ultimate source of the biological diversity on which natural selection acts, but the vast majority of these mutations are harmful. As such, mutations lead to disease states like cancer, extinction of small populations, and can drive pathogen evolution. Unfortunately, because mutations are rare and past studies have been subject to detection biases, very little is known about the distribution of fitness effects from naturally occurring mutations. In this study, we used mutation accumulation and full genome sequencing to capture naturally occurring mutations before they were exposed to the sieve of natural selection in Vibrio fischeri. We then measured the effects of these mutations on the fitness of the individuals harboring these mutations. We hypothesized that most mutations would be deleterious, and that deletions and insertions would be more detrimental to fitness than base substitutions, particularly in coding regions. Additionally, we expected to show that mutations on primary chromosomes, which are more highly expressed and evolutionarily conserved, would have more harmful effects than mutations on accessory secondary chromosomes. Using a subset of eleven mutation accumulation isolates, each harboring between two and nine mutations, we show that the majority of mutations have minor deleterious effects, with a subset of those errors resulting in more drastic fitness declines. However, extending this study to more genotypes will be required to examine the relationship between particular mutation types and fitness. Ultimately, an enhanced understanding of the relationship between genotype and fitness will broaden our understanding of the distribution of mutational effects and elucidate the susceptibility of different genome regions to deleterious variation.