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Epigenetic response to nanopolystyrene in germline of nematode Caenorhabditis elegans
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Germline microRNA mir-38 was found to be upregulated in the nematode C. elegans following exposure to 100-nm polystyrene nanoplastics, triggering an epigenetic response that reduced expression of downstream regulatory genes. This miRNA-mediated pathway represents a novel epigenetic mechanism by which nanoplastic exposure propagates molecular changes in reproductive tissues.
microRNAs (miRNAs) provide an epigenetic regulation mechanism for the response to environmental toxicants. mir-38, a germline miRNA, was increased by exposure to nanopolystyrene (100 nm). In this study, we further found that germline overexpression of mir-38 decreased expressions of nhl-2 encoding a miRISC cofactor, ndk-1 encoding a homolog of NM23-H1, and wrt-3 encoding a homolog of PPIL-2. Meanwhile, germline-specific RNAi knockdown of nhl-2, ndk-1, or wrt-3 caused the resistance to nanopolystyrene toxicity. Additionally, mir-38 overexpression suppressed the resistance of nematodes overexpressing germline nhl-2, ndk-1, or wrt-3 containing 3'UTR, suggesting the role of NHL-2, NDK-1, and WRT-3 as the targets of germline mir-38 in regulating the response to nanopolystyrene. Moreover, during the control of response to nanopolystyrene, EKL-1, a Tudor domain protein, was identified as the downstream target of germline NHL-2, kinase suppressors of Ras (KSR-1 and KSR-2) were identified as the downstream targets of germline NDK-1, and ASP-2, a homolog of BACE1, was identified as the downstream target of germline WRT-3. Our results raised a mir-38-mediated molecular network in the germline in response to nanopolystyrene in nematodes. Our data provided an important basis for our understanding the response of germline of organisms to nanoplastic exposure.
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Researchers used the model organism C. elegans to investigate how nanoplastic exposure causes transgenerational toxicity through effects on germline microRNA. The study found that polystyrene nanoparticles decreased expression of germline miRNA mir-38, and that overexpressing this miRNA conferred resistance to transgenerational toxicity. The findings suggest that nanoplastics can cause heritable toxic effects across generations by disrupting germline gene regulation.
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Researchers showed that polystyrene nanoplastics at environmentally predicted doses suppress germline histone acetyltransferases and deacetylases in C. elegans, and that silencing these chromatin-regulating enzymes worsened toxicity across multiple generations by dysregulating signaling ligands — identifying histone deacetylase inhibition as the molecular initiating event in an epigenetic adverse outcome pathway.
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