Activation of a G protein–coupled receptor by its endogenous ligand triggers the innate immune response of Caenorhabditis elegans. (Nature Immunology(2014) doi:10.1038/ni.2957)

報告日期: 2014/10/28
報告時間: 4:00/4:50
報告學生: 陳怡偉(以英文報告)
講評老師: 陳振暐
附件下載: 下載[1433-1412237692-1.pdf] 

Activation of a G protein–coupled receptor by its endogenous ligand triggers the innate immune response of

Caenorhabditis elegans

Olivier Zugasti, Neelanjan Bose, Barbara Squiban, Jérôme Belougne, C Léopold Kurz, Frank C Schroeder, Nathalie Pujol & Jonathan J Ewbank

 

Speaker:陳怡偉                                              Time2014/10/28 16:00

Commentator:陳振暐老師                 PlaceRoom 602

 

Abstract

G protein–coupled receptor (GPCR) is one of the most popular targets in therapeutic design. Studies have showed that drug discovery spend lots of time and cost. By using the nematode Caenorhabditis elegans, the long journey of drug discovery become faster and more convenient. Based on their previous study in fungi infection and wounding, the authors established an RNAi screen and identified the GPCR, DCAR-1. DCAR-1 is an epidermis specific GPCR that acts upstream of the conserved p38 MAPK pathway, triggering the expression of antimicrobial peptide NLP-29. For the understanding of the ligand which binds to DCAR-1, the authors analyzed metabolites and identified the tyrosine derivative 4-hydroxyphenyllactic acid (HPLA) as an endogenous ligand to DCAR-1. The finding of the ligand-receptor pair reveals HPLA-DCAR-1 is activated in the epidermis and control the innate immunity in fungi infection and wounding in C. elegans.

 

Reference

  1. Katja Ziegler, C Léopold Kurz, Sophie Cypowyj, Carole Couillault, Matthieu Pophillat, Nathalie Pujol & Jonathan J Ewbank (2009) Antifungal innate immunity in C. elegans: PKCdelta links G protein signaling and a conserved p38 MAPK cascade. Cell Host Microbe 5, 341–352.