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

[This corrects the article 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.

Table 2

C. elegans strains used in this study.

Strain name	Genotype/allele designation	Relevant characteristics	Source or reference
N2 Bristol	C. elegans wild isolate	Wild type isolate	CGCa
CU1546	smIs34	ced-1p::ced-1::GFP + rol-6(su1006)	CGCa
CB1370	daf-2(e1370) III	Mutated in the insulin-like receptor DAF-2. Temperature sensitive dauer constitutive	CGCa
IU10	daf-16(mgDf47) I; rrf-3(pk1426) II	Mutated in the FOXO-family transcription factor DAF-16	CGCa
TJ356	zIs356 IV	Integrated DAF-16::GFP roller strain. Daf-c, Rol, fluorescent DAF-16::GFP. Overexpression of DAF-16	CGCa
JT9609	pdk-1 (Sa680) x	Mutation in the gene encoding for 3-phosphoinositide-dependent protein kinase	CGCa
RB1178	wwp-1(ok1102) I.	Mutation in the gene encoding for the WW domain protein 1	CGCab
TM127	daf-2(e1370) III; sod-3(sj134) X	Double mutant in the insulin-like receptor DAF-2 and in the superoxide dismutase SOD-3	CGCa
GA186	sod-3(tm760) X	Mutated in the iron/manganese superoxide dismutase SOD-3	CGCa
RB1286	lys-7(ok1384) V	Mutated in the putative antimicrobial lysozyme LYS-7	CGCa
RB2045	spp-1(ok2703) III	Mutated in the antimicrobial peptide caenopore SPP-1	CGCa

a Caenorhabditis Genetics Center, the University of Minnesota.

b C. elegans Gene Knockout Project http://www.celeganskoconsortium.omrf.org.

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.

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

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