The neurotransmitter l-glutamate (Glu) plays a powerful role in many biological functions including behavior, lifespan, and metabolism. Glutamate transporters mediate extracellular Glu accumulation among neurons and glia to prevent excitotoxic neurotransmission and consequent neuronal damage and cell death. The effect of singular transporter deletion on behavior, lifespan, and proteomics remains largely unexplored despite extensive research on glutamatergic signaling pathways, so we knocked out Glt-4 and Glt-5 in the invertebrate Caenorhabditis elegans. Glt-5 mutant strains demonstrated minimal behavioral divergences with wildtype in sharp contrast to severe behavioral deficits observed in Glt-4 mutants. We also investigated the role of GluTs in mediating C. elegans lifespan characteristics. Glt-4 mutants exhibited decreased lifespan while Glt-5 mutants had increased longevity when both were compared to wildtype C. elegans. A global mass-spectrometry based approach identifed changes in protein expression that may account for the increased longevity precipitated by Glt-5 deletion. Proteomic results showed Glt-5 deletion affects a number of enzymes related to metabolism, stress response, cellular structure, movement, and development. Remarkably, the Glt-5 mutant strain expresses considerable upregulation of specific metabolic genes. We propose that Glt-5 mutants both optimize and maintain integral cellular functions above baseline levels as deletion of Glt-5 incites favorable changes in the C. elegans proteome.