Abstract

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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