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Acetylation regulation associated with the induction of protective response to polystyrene nanoparticles in Caenorhabditis elegans
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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.
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