Expression Levels of the Immune-Related p38 Mitogen-Activated Protein Kinase Transcript in Response to Environmental Pollutants on Macrophthalmus japonicus Crab

Abstract

Environmental pollution in the aquatic environment poses a threat to the immune system of benthic organisms. The Macrophthalmus japonicus crab, which inhabits tidal flat sediments, is a marine invertebrate that provides nutrient and organic matter cycling as a means of purification. Here, we characterized the M. japonicus p38 mitogen-activated protein kinase (MAPK) gene, which plays key roles in the regulation of cellular immune and apoptosis responses. M. japonicusp38 MAPK displayed the characteristics of the conserved MAPK family with Thr-Gly-Tyr (TGY) motif and substrate-binding site Ala-Thr-Arg-Trp (ATRW). The amino acid sequence of the M. japonicus p38 MAPK showed a close phylogenetic relationship to Eriocheir sinensis MAPK14 and Scylla paramamosainp38 MAPK. The phylogenetic tree displayed two origins of p38 MAPK: crustacean and insect. The tissue distribution patterns showed the highest expression in the gills and hepatopancreas of M. japonicus crab. In addition, p38 MAPK expression in M. japonicus gills and hepatopancreas was evaluated after exposure to environmental pollutants such as perfluorooctane sulfonate (PFOS), irgarol, di(2-ethylhexyl) phthalate (DEHP), and bisphenol A (BPA). In the gills, p38 MAPK expression significantly increased after exposure to all concentrations of the chemicals on day 7. However, on day 1, there were increased p38 MAPK responses observed after PFOS and irgarol exposure, whereas decreased p38 MAPK responses were observed after DEHP and BPA exposure. The upregulation of p38 MAPK gene also significantly led to M. japonicus hepatopancreas being undertested in all environmental pollutants. The findings in this study supported that anti-stress responses against exposure to environmental pollutants were reflected in changes in expression levels in M. japonicusp38 MAPK signaling regulation as a cellular defense mechanism.