First Advisor

Suzanne Estes

Date of Award


Document Type


Degree Name

Bachelor of Science (B.S.) in Biology and University Honors




Caenorhabditis elegans -- Fluorescence, Mitochondrial DNA, Mutation (Biology), Cells -- Aging, Cell death




Despite considerable research, the patterns and causes of senescence (biological aging) and organismal death are still mysterious. Evidence has been presented that organismal death in the nematode, Caenorhabitis elegans, is accompanied by a burst of blue "death fluorescence" (DF), which is generated within intestinal cells by the necrotic cell death pathway [1]. This blue death fluorescence has overlapping activity with uranin fluorescence which can act as a marker for loss of membrane integrity in lysosome related organelles due to the fact it is quenched at low pH. It has been proposed that dequenching of uranin fluorescence upon gut granule permeabilization leads to a burst of green fluorescence in C. elegans [1]. This paper aims to investigate whether mitochondrial dysfunction, as represented by the gas-1 (fc21) gene mutation, leads to a different pattern of age related uranin fluorescence when compared to wildtype. In order to measure uranin fluorescence, a Leica confocal microscope was used to image age-synchronous samples of gas-1 compensatory recovery line worms as well as gas-1, progenitor, and N2 ,wildtype, worms dyed with fluorescein sodium salt at three different time points in their life cycle. Results should indicate whether there is a difference in age-related patterns of uranin fluorescence between the gas-1 lines as compared to wildtype. Using relative fitness data, inferences might also be able to be made regarding patterns of uranin fluorescence and fitness among the gas-1 compensatory recovery lines themselves.


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