We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Acetylation regulation associated with the induction of protective response to polystyrene nanoparticles in Caenorhabditis elegans
Summary
Researchers found that polystyrene nanoparticle exposure in C. elegans upregulates CBP-1, a histone acetyltransferase, which orchestrates a protective epigenetic response across intestinal, neuronal, and germline tissues by modulating insulin, p38 MAPK, TGF-β, and JNK signaling pathways to counteract nanoplastic toxicity.
Caenorhabditis elegans is a useful animal model to assess nanoplastic toxicity. Using polystyrene nanoparticles (PS-NPs) as the example of nanoplastics, we found that exposure to PS-NPs (1-100 μg/L) from L1-larvae for 6.5 days increased expression of cbp-1 encoding an acetyltransferase. The susceptibility to PS-NPs toxicity was observed in cbp-1(RNAi) worms, suggesting that CBP-1-mediated histone acetylation regulation reflects a protective response to PS-NPs. The functions of CBP-1 in intestine, neurons, and germline were required for formation of this protective response. In intestinal cells, CBP-1 controlled PS-NPs toxicity by modulating functions of insulin and p38 MAPK signaling pathways. In neuronal cells, CBP-1 controlled PS-NPs toxicity by affecting functions of DAF-7/TGF-β and JNK MAPK signaling pathways. In germline cells, CBP-1 controlled PS-NPs toxicity by suppressing NHL-2 activity, and NHL-2 further regulated PS-NPs toxicity by modulating insulin communication between germline and intestine. Therefore, our data suggested that the CBP-1-mediated histone acetylation regulation in certain tissues is associated with the induction of protective response to PS-NPs in C. elegans.