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Open Access

Correction

Correction: Antinematode Activity of Violacein and the Role of the Insulin/IGF-1 Pathway in Controlling Violacein Sensitivity in Caenorhabditis elegans

  • Francesco Ballestriero,
  • Malak Daim,
  • Anahit Penesyan,
  • Jadranka Nappi,
  • David Schleheck,
  • Paolo Bazzicalupo,
  • Elia Di Schiavi,
  • Suhelen Egan

There is an error in the eleventh paragraph of the Results section. The correct paragraph is: In C. elegans DAF2/DAF16 controls the expression of various effector genes including those relevant for detoxification and antimicrobial activity such as the superoxidase dismutase gene sod-3 and antimicrobial genes spp-1 and lys-7 [23,38]. Thus given that the precise molecular target/s for violacein in C. elegans are unknown we sought to determine which, if any, of these relevant downstream genes are required for the increased resistance to violacein observed in daf-2 null and DAF-16 over-expressing strains. Specifically we chose to test violacein sensitivity in C. elegans mutants defective in sod-3, spp-1 and lys-7 (Table 2) because of the previous reported involvement of these genes in immunity to bacterial accumulation [39,40,41]. We found that daf-2;sod-3 double mutant displayed significantly reduced survival compared to the single mutant daf-2 (p<0.0001, Fig 6A) when exposed to the 20G8 clone in a nematode killing assay. Interestingly a single mutation in gene spp-1 significantly reduced the nematode’s life span when compared to wild type animals (p<0.0001), while the viability of the nematode was not affected by mutations in the lys-7 and sod-3 genes (p>0.05, Fig 6B). These data indicate that resistance to violacein in daf-2 mutants is at least in part driven by SPP-1 and SOD-3, with the antimicrobial LYS-7 having little or no involvement.

Fig 6 is incorrect. Please see the corrected Fig 6 here.

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Fig 6. Nematode killing assay (wild type animals and daf-2, daf-2;sod-3, spp-1, lys-7, sod-3 mutant nematodes vs the 20G8 clone).

(A) The survival of the nematode was tested using C. elegans double mutant daf-2;sod-3, and (B) the single mutant animals sod-3, spp-1, and lys-7. Each data point represents means ± the standard error of three replicate plates. p values were calculated on the pooled data of all of the plates done in each experiment by using the log-rank (Mantel–Cox) method and the values are provided in the text.

https://doi.org/10.1371/journal.pone.0210026.g001

Table 2 is incorrect. Please see the corrected Table 2 here.

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Table 2. C. elegans strains used in this study.

https://doi.org/10.1371/journal.pone.0210026.t001

Reference

  1. 1. Ballestriero F, Daim M, Penesyan A, Nappi J, Schleheck D, Bazzicalupo P, et al. (2014) Antinematode Activity of Violacein and the Role of the Insulin/IGF-1 Pathway in Controlling Violacein Sensitivity in Caenorhabditis elegans. PLoS ONE 9(10): e109201. https://doi.org/10.1371/journal.pone.0109201 pmid:25295516

Citation: Ballestriero F, Daim M, Penesyan A, Nappi J, Schleheck D, Bazzicalupo P, et al. (2018) Correction: Antinematode Activity of Violacein and the Role of the Insulin/IGF-1 Pathway in Controlling Violacein Sensitivity in Caenorhabditis elegans. PLoS ONE 13(12): e0210026. https://doi.org/10.1371/journal.pone.0210026

Published: December 26, 2018

Copyright: © 2018 Ballestriero et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.