Publication Date


Document Type


First Advisor

Blackstone, Neil W.

Degree Name

M.S. (Master of Science)

Legacy Department

Department of Biological Sciences


Biological complexity forms when lower-level units (e.g., genes, cells, organisms) cooperatively band together. This complexity may be exemplified by multicellularity, the cooperation between the cells of the same species, or symbiosis, cooperation between the cells of different species. This cooperation is under continual threat, as defection, the opposite of cooperation, is favored by default by lower-level units (i.e., cells). Animal cancers may be the most well-known phenomena that exemplify the concept of cellular defection. Cancer cells have been shown to feature morphological and metabolic traits, developed through differential gene expression or mutations, that favor their growth at the cost of the higher-level unit (i.e., the organism). For instance, the Warburg effect is the observation that most cancer cells are characterized by an increase in the glucose uptake rate and preferential production of lactate, even in the presence of oxygen. Understanding the mechanisms that govern cancers' morphological and metabolic traits can be enhanced through a more generalized context (e.g., the evolution of cooperation). Colonial cnidarians may provide convenient models for insight into how conflict mediation mechanisms may favor cellular cooperation's evolution. This study aimed to provide insight into how nutrient scarcity affects the growth, energy metabolism, and mutation rates of the clonal hydroid: Eirene viridula. Two groups of E. viridula colonies defined by differential feeding treatments were grown from the same founder colony under artificial laboratory environments. After their growth period, the two groups were measured and compared for various response variables relating to colony morphology, energy metabolism, and replication/mutation rate. The nutrient-abundant group featured a significantly higher replication rate than the nutrient-scarce group. Neither of the experimental groups featured single nucleotide polymorphisms (SNPs) when assessed from five genetic (three nuclear and two mitochondrial) fragments. The nutrient-abundant group featured more clumped or 'sheet-like' colony morphologies than the nutrient-scarce group, which parallel cancer tumors' dense, localized growth. The nutrient-scarce colonies featured suggestively higher size-adjusted measures of oxygen uptake, which may signify an upregulated chemiosmotic metabolism. These results suggest that the levels of nutrients may have major implications for the development of metabolic traits that characterize cancer cells. Further research is needed to elucidate the genetics or signaling pathways that cause these metabolic shifts.


47 pages




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