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


Christopher G. James, Ofodile Morah, Victoria Panwala, Amin Yarmand​

Volume 4
Fall 2017 / Winter 2018

SUMMARY 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 Caenorhabditis elegans pathogen, Pseudomonas aeruginosa. Inhibition of the dopamine signaling pathway has been found to increase survival of Caenorhabditis elegans infected with Pseudomonas aeruginosa via activation of the p38/MAPK pathway. It is not known whether loss of dopamine signaling affects Escherichia coli infection of Caenorhabditis elegans. Here, we aimed to investigate the effect of putative inhibition of dopamine signaling on the nematode survivability against Escherichia 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 Pseudomonas aeruginosa infection. Using a 10 or 12- day survival assay, we compared survival of Caenorhabditis elegans wild type (WT) Bristol N2 strain and a dop-1 mutant strain of Caenorhabditis 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 Caenorhabditis 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 Caenorhabditis 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 Escherichia coli infection model in Caenorhabditis elegans in an undergraduate laboratory setting and confirms the previous findings that O antigen expressing Escherichia coli is pathogenic to Caenorhabditis elegans. Moreover, the data indicates that treatment of Caenorhabditis elegans with CPZ and a missense mutation in dop-1 does not provide protection to DFB1655 infection.