Survival of Caenorhabditis elegans Infected with Escherichia coli DFB1655 is not Affected by a Missense Mutation in dop-1 or Treatment with Chlorpromazine Hydrochloride

Abstract

The O antigen producing Escherichia coli strain DFB1655 L9 has been shown to be pathogenic to Caenorhabditis elegans, with killing rates comparable to the known C. elegans pathogen, Pseudomonas aeruginosa. Inhibition of the dopamine signaling pathway has been found to increase survival of C. elegans infected with P. aeruginosa via activation of the p38/MAPK pathway. It is not known whether loss of dopamine signaling affects E. coli infection of C. elegans. Here, we aimed to investigate the effect of putative inhibition of dopamine signaling on the nematode survivability against E. coli DFB1655 L9 infection. We hypothesized that successful attempts at inhibiting dopamine signaling would protect nematodes against DFB1655 infection based on previously reported results from P. aeruginosa infection. Using a 10 or 12-day survival assay, we compared survival of C. elegans wild type (WT) Bristol N2 strain and a dop-1 mutant strain of C. elegans with a missense mutation in D-1 like dopamine receptor against DFB1655 infection. Chlorpromazine hydrochloride was also used as a dopamine receptor antagonist in WT worms. Our results show that C. elegans have a significantly lower survival percentage over time when growing on DFB1655 compared to growth on the parent MG1655 strain. Moreover, dop-1 mutant C. elegans showed no enhanced survivability compared to WT worms infected with DFB1655 L9. No increased survival over time was observed in CPZ-treated WT worms compared to the water-treated controls. This study establishes an E. coli infection model in C. elegans in an undergraduate laboratory setting and confirms previous findings that O antigen-expressing E. coli is pathogenic to C. elegans. Moreover, the data indicates that treatment of C. elegans with CPZ and a missense mutation in dop-1 does not provide protection to DFB1655 infection.