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. 2018 Mar 19;9(1):683–699. doi: 10.1080/21505594.2018.1438025

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© 2018 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 2. — BAR-1, FSHR-1, and PMK-1 are required for defense against both E. faecalis and E. faecium. (A, B) Survival of wild-type N2, pmk-1(km25), fshr-1(ok778), and pmk-1(km25);fshr-1(ok778) C. elegans on E. faecalis (left) and wild-type N2, pmk-1(km25), bar-1(ga80), and pmk-1(km25);bar-1(ga80) animals (right) on E. faecalis (A) and E. faecium (B), sterilized with cdc-25.1 RNAi. (C) Survival of N2 and pmk-1(km25) worms sterilized with cdc-25.1 RNAi on heat-killed E. faecalis. Each graph shows the average of three plates for each strain, with each plate containing 30–40 worms. Results are representative of 3 independent assays. Statistical significance of differences between survival curves was calculated using Kaplan-Meier log rank analysis. Strains that showed a statistically significant difference from N2 are denoted with an asterisk and bracket. (D) Bacterial load of wild-type N2 and pmk-1 C. elegans after infection with E. faecalis or E. faecium. Time course of colony forming units in the intestines of wild-type N2 or pmk-1 deficient C. elegans, sterilized with cdc-25.1, and infected with either E. faecalis or E. faecium. Error bars represent the standard deviation. Results are representative of 2 independent assays; each condition of each experiment was performed in triplicate or quadruplicate.