Correction: Antinematode activity of violacein and the role of the insulin/IGF-1 pathway in controlling violacein sensitivity in caenorhabditis elegans (PLoS One (2014) 9:10 (e109201) DOI: 10.1371/journal.pone.0109201)

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. (Figure Presented) (Table Presented).