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Exposure to graphene oxide (GO) induced some dysregulated microRNAs (miRNAs), such as the increase in  mir-247 , in nematode  Caenorhabditis elegans . We here further identified  goa-1  encoding a Gαo and  pkc-1  encoding a serine/threonine protein kinase as the targets of neuronal  mir-247  in the regulation of GO toxicity. GO exposure increased the expressions of both GOA-1 and PKC-1. Mutation of  goa-1  or  pkc-1  induced a susceptibility to GO toxicity, and suppressed the resistance of  mir-247  mutant to GO toxicity. GOA-1 and PKC-1 could also act in the neurons to regulate the GO toxicity, and neuronal overexpression of  mir-247  could not affect the resistance of nematodes overexpressing neuronal  goa-1  or  pkc-1  lacking 3′-UTR to GO toxicity. In the neurons, GOA-1 acted upstream of diacylglycerol kinase/DGK-1 and PKC-1 to regulate the GO toxicity. Moreover, DGK-1 and GOA-1 functioned synergistically in the regulation of GO toxicity. Our results highlight the crucial role of neuronal Gαo signaling in response to GO in nematodes.

Dysregulation of Neuronal Gαo Signaling by Graphene Oxide in Nematode Caenorhabditis elegans