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Shante L. Hutchinson Biology Department North Carolina A&T State University

Testing the Life History Theory Predictions of Trade-offs Between Reproductive Rate and Life Span in Yeast. Shante Hutchinson and Barry Williams, Ph.D 2 ., 1 Biology Department and North Carolina A&T State University, 2 Zoology Department Michigan State University. RESULTS. ABSTRACT.

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Shante L. Hutchinson Biology Department North Carolina A&T State University

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  1. Testing the Life History Theory Predictions of Trade-offs Between Reproductive Rate and Life Span in Yeast Shante Hutchinson and Barry Williams, Ph.D2.,1Biology Department and North Carolina A&T State University, 2Zoology Department Michigan State University RESULTS ABSTRACT INTRODUCTION Yeast (Saccharomyces cerevisiae) is one of the most highly researched organisms in biology because of their use in the industry and their central role as a model organism for basic research. Chronological aging, defined as the length of time a dormant cell remains viable, and cellular proliferation are both intensively studied using the yeast model system. Chronological aging and reproductive rates are thought to have a trade-off due to antagonistic pleiotropy. This study will determine whether an antagonistic pleiotropic trade-off between reproduction and lifespan exists in S. cerevisiae. Top figure: difference in chronological age between a control strain versus several mutant strains (mut) with increased reproductive rates (measured as faster growth in the presence of the antifungal drug Fluconazole). The bottom two figures illustrate growth rate measurements for cells: left figure - average time to reach midlog phase of growth for two strains; right figure - growth curves measured as the optical density of cultures at a wavelength of 630 nanometers (OD630) every 20 minutes. The results in the top figure demonstrate that strains with higher growth rates also have increased chronological lifespan, I.e., they are aging faster than the control. Increased lifespan would seem to be a beneficial trait, but mutations that increase life span are often found in genetic screens, meaning that the evolution of increased lifespan is possible but has not occurred. Previous research in life history theory suggests that increased lifespan is a trade-off against lower reproductive rates, likely because both traits are controlled by the same genes, i.e. antagonistic pleiotropy. Despite abundant evidence in support of antagonistic pleiotropy, this trade-off has never been examined in the unicellular eukaryote Saccharomyces cerevisiae. Here we tested whether a pleiotropic trade-off between reproductive rate and senescence exists in S. cerevisiae. If so, the molecular genetic tools available in this study system can subsequently help identify the mechanism responsible for the trade-off between reproduction and life span. METHODS AND MATERIALS CONCLUSIONS FUTURE WORK • Isolation of strains with adaptive mutations that increased reproductive rate, or cellular proliferation, was possible. • Determined that there is an existence of trade-offs between reproduction and lifespan in Saccharomyces cerevisiae. • This research helped identify the molecular genetic mechanisms for the trade-off between reproduction and life span in yeast. • Identify and characterize the mutations that cause the observed trade-offs • Determine the molecular mechanisms behind senescence and reproduction • Identify the link between reproduction and senescence trade-offs. CONTACT Shante L. HutchinsonBiology Department North Carolina A&T State University slhutchi@aggies.ncat.edu REFERENCES Longo, V., Shadel, G., Kaeberlein, M., “Replicative and Chronological Aging in Saccharomyces cerevisiae,” Elsevier Incorporated, Cell Metabolism Volume 16, 2012, pp. 18-31. Diezmann, S., Dietrich, F., “Oxidative Stress Survival in a Clinical Saccharomyces cerevisae Isolate Is Influenced by a Major Quantitative Trait Nucleotide” Genetics Journal, Vol. 1, 1883, pp. 709-722. Warringer, J., Zorgo, E., Cubillos, F., “Trait Variation in Yeast is Defined by Population History,” PLOS Genetics ,2011, pp. 512-524

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