Long-term and low-dose exposure to nanopolystyrene induces a protective strategy to maintain functional state of intestine barrier in nematode Caenorhabditis elegans.

Functional state of intestinal barrier plays an important role for environmental animals in being against various toxicants. We investigated GATA transcriptional factor ELT-2-mediated intestinal response to nanopolystyrere in Caenorhabditis elegans. Prolonged exposure to nanopolystyrene (≥1 μg/L) induced an increase in expression of ELT-2, and intestinal RNA interference (RNAi) knockdown of elt-2 caused enhancement in intestinal permeability. Meanwhile, mutation of elt-2 resulted in susceptibility to nanopolystyrene toxicity, and ELT-2 functioned in intestine to regulate the nanopolystyrene toxicity. ERM-1, CLEC-63, and CLEC-85 were identified as targets of ELT-2 in regulating the nanopolystyrene toxicity. ERM-1 was required for maintaining functional state in intestinal barrier, and functioned synergistically with CLEC-63 or CLEC-85 to regulate nanopolystyrene toxicity. Therefore, activation of intestinal ELT-2 by nanopolystyrere could mediate a protective strategy to maintain the functional state of intestinal barrier. During this process, intestinal ELT-2 activated two different molecular signals (ERM-1 signal and CLEC-63/85 signal) for nematodes against the nanopolystyrene toxicity.