Multi-walled carbon nanotubes induce transgenerational toxicity associated with activation of germline long non-coding RNA linc-7 in C. elegans

With the increase in application, multi-walled carbon nanotubes (MWCNTs) are potentially bioavailable to environmental organisms. However, the potential transgenerational effect of MWCNTs and underlying mechanisms remains still unclear. Here, we examined transgenerational MWCNT toxicity and the underlying mechanism mediated by germline long non-coding RNAs (lncRNAs) in Caenorhabditis elegans. Exposure to 0.1-10 mu g/L MWCNT caused transgenerational toxicity reflected by endpoints of brood size and locomotion behavior. Meanwhile, among germline lncRNAs, expression of 5 lncRNAs were dysregulated by MWCNT exposure. Among these 5 dysregulated lncRNAs, only germline RNAi of linc-7 affected MWCNT toxicity. Increase in germline linc-7 expression was observed transgenerationally, and transgenerational MWCNT toxicity was prevented in linc-7 (RNAi) nematodes. Moreover, germline linc-7 controlled transgenerational MWCNT toxicity by activating downstream DAF-12, a transcriptional factor. Therefore, our data indicated the association between induction of transgenerational MWCNT toxicity and increase in germline linc-7 expression in organisms.

Automated summary

This study investigated the transgenerational toxicity of multi-walled carbon nanotubes (MWCNTs) and the role of germline long non-coding RNAs (lncRNAs) in Caenorhabditis elegans. The results showed that exposure to MWCNTs caused transgenerational toxicity in terms of decreased brood size and impaired locomotion behavior. Among germline lncRNAs, expression of 5 lncRNAs was dysregulated by MWCNT exposure. Further analysis revealed that only germline RNAi of linc-7 affected MWCNT toxicity. Germline linc-7 expression was increased transgenerationally, and transgenerational MWCNT toxicity was prevented in linc-7 (RNAi) nematodes. Additionally, germline linc-7 controlled transgenerational MWCNT toxicity by activating downstream transcription factor DAF-12.