Regulation of Innate Immune Response to Fungal Infection in Caenorhabditis elegans by SHN-1/SHANK

• Published in: Journal of microbiology and biotechnology 2020, 30(11), , pp.1626-1639
• Main Authors: Sun, Lingmei, Li, Huirong, Zhao, Li, Liao, Kai
• Format: Article
• Language: English
• Subjects: Research article; 생물학
• ISSN: 1017-7825; 1738-8872
• DOI: 10.4014/jmb.2006.06025

In Caenorhabditis elegans , SHN-1 is the homologue of SHANK, a scaffolding protein. In this study, we determined the molecular basis for SHN-1/SHANK in the regulation of innate immune response to fungal infection. Mutation of shn-1 increased the susceptibility to Candida albicans infection and suppressed the innate immune response. After C. albicans infection for 6, 12, or 24 h, both transcriptional expression of shn-1 and SHN-1::GFP expression were increased, implying that the activated SHN-1 may mediate a protection mechanism for C. elegans against the adverse effects from fungal infection. SHN-1 acted in both the neurons and the intestine to regulate the innate immune response to fungal infection. In the neurons, GLR-1, an AMPA ionotropic glutamate receptor, was identified as the downstream target in the regulation of innate immune response to fungal infection. GLR-1 further positively affected the function of SER-7-mediated serotonin signaling and antagonized the function of DAT-1-mediated dopamine signaling in the regulation of innate immune response to fungal infection. Our study suggests the novel function of SHN-1/SHANK in the regulation of innate immune response to fungal infection. Moreover, our results also denote the crucial role of neurotransmitter signals in mediating the function of SHN-1/SHANK in regulating innate immune response to fungal infection.