Modulatory upregulation of an insulin peptide gene by different pathogens in <i>C. elegans</i> Song-Hua Lee Shizue Omi Nishant Thakur Clara Taffoni Jérôme Belougne Ilka Engelmann Jonathan J. Ewbank Nathalie Pujol 10.6084/m9.figshare.7491989.v1 https://tandf.figshare.com/articles/dataset/Modulatory_upregulation_of_an_insulin_peptide_gene_by_different_pathogens_in_i_C_elegans_i_/7491989 <p>When an animal is infected, its innate immune response needs to be tightly regulated across tissues and coordinated with other aspects of organismal physiology. Previous studies with <i>Caenorhabditis elegans</i> have demonstrated that insulin-like peptide genes are differentially expressed in response to different pathogens. They represent prime candidates for conveying signals between tissues upon infection. Here, we focused on one such gene, <i>ins-11</i> and its potential role in mediating cross-tissue regulation of innate immune genes. While diverse bacterial intestinal infections can trigger the up-regulation of <i>ins-11</i> in the intestine, we show that epidermal infection with the fungus <i>Drechmeria coniospora</i> triggers an upregulation of <i>ins-11</i> in the epidermis. Using the <i>Shigella</i> virulence factor OpsF, a MAP kinase inhibitor, we found that in both cases, <i>ins-11</i> expression is controlled cell autonomously by p38 MAPK, but via distinct transcription factors, STA-2/STAT in the epidermis and HLH-30/TFEB in the intestine. We established that <i>ins-11</i>, and the insulin signaling pathway more generally, are not involved in the regulation of antimicrobial peptide gene expression in the epidermis. The up-regulation of <i>ins-11</i> in the epidermis does, however, affect intestinal gene expression in a complex manner, and has a deleterious effect on longevity. These results support a model in which insulin signaling, via <i>ins-11</i>, contributes to the coordination of the organismal response to infection, influencing the allocation of resources in an infected animal.</p> 2018-12-20 14:43:34 fungus Drechmeria coniospora triggers p 38 MAPK insulin peptide gene insulin-like peptide genes Shigella virulence factor OpsF antimicrobial peptide gene expression ins -11 expression HLH MAP kinase inhibitor infection epidermis C . elegans ins -11 STA response