Arsenic is the most ubiquitous environmental toxin. Bacteria have evolved the ability to use arsenic to gain a competitive advantage over other bacteria at least twice. Microbes generate toxic methylarsenite (MAs(III)) by methylation of arsenite (As(III)) or reduction of methylarsenate (MAs(V)). MAs(III) is oxidized aerobically to MAs(V), making methylation a detoxification process. MAs(V) is continually re-reduced to MAs(III) by other community members, giving them a competitive advantage over sensitive bacteria. Because generation of a sustained pool of MAs(III) requires microbial communities, these complex interactions are an emergent property. We show that reduction of MAs(V) by Burkholderia sp. MR1 produces toxic MAs(III) that inhibits growth of Escherichia coli in mixed culture. There are three microbial mechanisms for resistance to MAs(III). ArsH detoxifies MAs(III) by oxidation to nontoxic MAs(V). ArsI degrades MAs(III) by cleavage of the C-As bond to form less toxic As(III). ArsP confers resistance by efflux of MAs(III). Cells of E. coli expressing the MAs(III)-resistance gene arsI, arsH or arsP grow in mixed culture with Burkholderia sp. MR1 in the presence of MAs(V). Thus MAs(III) has antibiotic properties: a toxic organic compound produced by one microbe to kill off competitors. Our results demonstrate that life has adapted to use environmental arsenic as a weapon in the continuing battle for dominance. Supported by NIH grants GM55425 and ES023779 to BPR, and by NSF BIO/MCB Grant 1817962 to MY.