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Caenorhabditis elegans  is an important non-mammalian alternative assay model for toxicological study. Previous study has indicated that exposure to multi-walled carbon nanotubes (MWCNTs) dysregulated the transcriptional expression of  mir-259 . In this study, we examined the molecular basis for  mir-259  in regulating MWCNTs toxicity in nematodes. Mutation of  mir-259  induced a susceptible property to MWCNTs toxicity, and MWCNTs exposure induced a significant increase in  mir-259::GFP  in pharyngeal/intestinal valve and reproductive tract, implying that  mir-259  might mediate a protection mechanisms for nematodes against MWCNTs toxicity. RSKS-1, a putative ribosomal protein S6 kinase, acted as the target for  mir-259  in regulating MWCNTs toxicity, and mutation of  rsks-1  suppressed the susceptible property of  mir-259  mutant to MWCNTs toxicity. Moreover,  mir-259  functioned in pharynx-intestinal valve and RSKS-1 functioned in pharynx to regulate MWCNTs toxicity. Furthermore, RSKS-1 regulated MWCNTs toxicity by suppressing the function of AAK-2-DAF-16 signaling cascade. Our results will strengthen our understanding the microRNAs mediated protection mechanisms for animals against the toxicity from certain nanomaterials.

scientific reports

Function of RSKS-1-AAK-2-DAF-16 signaling cascade in enhancing toxicity of multi-walled carbon nanotubes can be suppressed by mir-259 activation in Caenorhabditis elegans