Induction of protective response to polystyrene nanoparticles associated with methylation regulation in Caenorhabditis elegans

The epigenetic regulation mechanisms for toxicity induction of nanoplastics in organisms remain largely unknown. In Caenorhabditis elegans, we found that prolonged exposure to 1-100 mu g/L polystyrene nanoparticles (PS-NPs) decreased expression of MET-2, a H3K9 methyltransferase. Meanwhile, RNAi knockdown of met-2 suppressed the PS-NPs toxicity in inducing production of reactive oxygen species (ROS) and in decreasing locomotion behavior, which suggesting that the decrease in MET-2 expression reflected a protective response. This resistance to PS-NPs toxicity could be further detected in worms with met-2 RNAi knockdown in both intestinal cells and germline cells. In PS-NPs exposed worms, intestinal RNAi knockdown of met-2 significantly increased expressions of daf-16, bar-1, and elt-2. Intestinal RNAi knockdown of daf-16, bar-1, or elt-2 suppressed the resistance of met-2(RNAi) worms to PS-NPs toxicity, suggesting that MET-2 functioned upstream of ELT-2, BAR-1, and DAF-16 in intestinal cells to control PS-NPs toxicity. Moreover, in PS-NPs exposed worms, germline RNAi knockdown of met-2 significantly decreased expressions of wrt-3 and pat-12. RNAi knockdown of wrt-3 or pat-12 further inhibited the susceptibility of worms overexpressing germline MET-2 to PS-NPs toxicity, suggesting that MET-2 functioned upstream of PAT-12 and WRT-3 in germline cells to control PS-NPs toxicity. Therefore, our data provided an important molecular basis for MET-2-mediated methylation regulation in causing protective response to nanoplastics in organisms. (C) 2021 Elsevier Ltd. All rights reserved.

Automated summary

The study revealed that exposure to polystyrene nanoparticles led to decreased expression of MET-2 in Caenorhabditis elegans, reflecting a protective response. This protective response was confirmed in both intestinal and germline cells. Furthermore, MET-2 was found to regulate the toxicity induction process of PS-NPs in intestinal cells and germline cells.