Antagonistic interactions are widespread in microbial communities, influencing not only the composition and relative proportions of their members but also their long-term stability. Microbes utilize various antagonistic mechanisms, such as producing broad-spectrum antibiotics or secreting narrow-spectrum proteinaceous toxins called bacteriocins. Our understanding of how these interactions shape the overall structure, dynamics, and composition of microbial communities is still in its infancy. This research advances our knowledge by genetically engineering Escherichia coli to secrete specific bacteriocins - microcins MccB17 and MccV - using chemically inducible promoters, enabling controlled investigations into the ecological and evolutionary dynamics of microbial antagonism at variable toxin production rates. This thesis will detail the engineering of two E. coli strains and the regulation of toxin gene expression. Future research will employ these strains to examine competitive antagonism's effects on coexistence and competitive exclusion in E. coli communities.