Literature DB >> 29080785

A conserved Toll-like receptor-to-NF-κB signaling pathway in the endangered coral Orbicella faveolata.

Leah M Williams1, Lauren E Fuess2, Joseph J Brennan1, Katelyn M Mansfield1, Erick Salas-Rodriguez1, Julianne Welsh1, Jake Awtry3, Sarah Banic3, Cecilia Chacko3, Aarthia Chezian3, Donovan Dowers3, Felicia Estrada3, Yu-Hsuan Hsieh3, Jiawen Kang3, Wanwen Li3, Zoe Malchiodi3, John Malinowski3, Sean Matuszak3, Thomas McTigue3, David Mueller3, Brian Nguyen3, Michelle Nguyen3, Phuong Nguyen3, Sinead Nguyen3, Ndidi Njoku3, Khusbu Patel3, William Pellegrini3, Tessa Pliakas3, Deena Qadir3, Emma Ryan3, Alex Schiffer3, Amber Thiel3, Sarah A Yunes3, Kathryn E Spilios3, Jorge H Pinzón C2, Laura D Mydlarz2, Thomas D Gilmore4.   

Abstract

Herein, we characterize the Toll-like receptor (TLR)-to-NF-κB innate immune pathway of Orbicella faveolata (Of), which is an ecologically important, disease-susceptible, reef-building coral. As compared to human TLRs, the intracellular TIR domain of Of-TLR is most similar to TLR4, and it can interact in vitro with the human TLR4 adapter MYD88. Treatment of O. faveolata tissue with lipopolysaccharide, a ligand for mammalian TLR4, resulted in gene expression changes consistent with NF-κB pathway mobilization. Biochemical and cell-based assays revealed that Of-NF-κB resembles the mammalian non-canonical NF-κB protein p100 in that C-terminal truncation results in translocation of Of-NF-κB to the nucleus and increases its DNA-binding and transcriptional activation activities. Moreover, human IκB kinase (IKK) and Of-IKK can both phosphorylate conserved residues in Of-NF-κB in vitro and induce C-terminal processing of Of-NF-κB in vivo. These results are the first characterization of TLR-to-NF-κB signaling proteins in an endangered coral, and suggest that these corals have conserved innate immune pathways.
Copyright © 2017 Elsevier Ltd. All rights reserved.

Entities:  

Keywords:  Coral; Evolution; Innate immunity; NF-kappaB; Orbicella faveolata; Toll-like receptor

Mesh:

Substances:

Year:  2017        PMID: 29080785     DOI: 10.1016/j.dci.2017.10.016

Source DB:  PubMed          Journal:  Dev Comp Immunol        ISSN: 0145-305X            Impact factor:   3.636


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