▎ 摘　　要

In nematode Caenorhabditis elegans, epidermal RNA interference (RNAi) knockdown of bli-1 encoding a cuticular collagen caused the toxicity induction of GO-PEG (PEG surface modified graphene oxide). In this study, we further found that epidermal RNAi knockdown of bli-1 increased expression of a microRNA let-7, and let-7 mutation suppressed the susceptibility of bli-1(RNAi) nematodes to GO-PEG toxicity. let-7 regulated the toxicity induction of GO-PEG by suppressing expression and function of its direct targets (HBL-1 and LIN-41). Like the nematodes with epidermal RNAi knockdown of bli-1, epidermal RNAi knockdown of hbl-1 or lin-41 also induced functional abnormality in epidermal barrier. Therefore, a signaling cascade of BLI-1-let-7-HBL-1/LIN-41 was raised to be involved in GO-PEG toxicity induction. Our data imply the dysregulation of let-7-mediated molecular machinery for developmental timing control by GO-PEG in nematodes with deficit in epidermal barrier caused by bli-1(RNAi).