Neuronal Gα subunits required for the control of response to polystyrene nanoparticles in the range of μg/L in C. elegans

The aim of this study was to identify G alpha proteins mediating function of neuronal G protein-coupled receptors (GPCRs) in controlling the response to polystyrene nanoparticles (PS-NPs). Caenorhabditis elegans was used as an animal model, and both gene expression and functional analysis were performed to identify the G alpha proteins in controlling PS-NPs toxicity. In nematodes, exposure to PS-NPs (1-100 mu g/L) significantly altered transcriptional expressions of some neuronal G alpha genes, including gpa-5, gpa-10, gpa-11, gpa-15 gsa-1, egl-30, and goa-1. Among these 7 G alpha genes, only neuronal RNAi knockdown of gsa-1, gpa-10, and goa-1 affected toxicity of PS-NPs in inducing ROS production and in decreasing locomotion behavior. Some neuronal GPCRs (such as GTR-1, DCAR1, DOP-2, NPR-8, NPR-12, NPR-9, and DAF-37) functioned upstream of GOA-1, some neuronal GPCRs (such as DCAR-1, DOP-2, NPR-9, NPR-8, and DAF-37) functioned upstream of GSA-1, and some neuronal GPCRs (such as DOP-2, NPR-8, DAF-37, and DCAR-1) functioned upstream of GPA-10 to regulate the toxicity of PS-NPs. Moreover, GOA-1 acted upstream of MPK-1/ERK MAPK, JNK-1/JNK MAPK, DBL-1/TGF-beta, and DAF-7/ TGF-beta, GSA-1 functioned upstream of MPK-1/ERK MAPK, JNK-1/JNK MAPK, and DBL-1/TGF-beta, and GPA-10 functioned upstream of GLB-1/Globin and DBL-1/TGF-beta to control the PS-NPs toxicity. Therefore, neuronal G alpha proteins of GOA-1, GSA-1, and GPA-10 functioned to transduce signals of multiple GPCRs to different downstream signaling pathways during the control of PS-NPs toxicity in nematodes. Our results provide clues for understanding the important function of GPCRs-G alpha signaling cascade in the neurons in controlling response to nanoplastics in organisms.

Automated summary

This study identified the roles of neuronal G alpha proteins GOA-1, GSA-1, and GPA-10 in controlling the response to polystyrene nanoparticles in nematodes. These proteins transduce signals from multiple GPCRs to different downstream signaling pathways, regulating toxicity effects. The findings emphasize the significance of GPCRs-G alpha signaling cascade in neurons for managing nanoplastic responses in organisms.