GONUTS has been updated to MW1.31 Most things seem to be working but be sure to report problems.

Have any questions? Please email us at ecoliwiki@gmail.com

TableEdit

Jump to: navigation, search

PMID:21575913

You don't have sufficient rights on this wiki to edit tables. Perhaps you need to log in. Changes you make in the Table editor will not be saved back to the wiki

See Help for Help on this wiki. See the documentation for how to use the table editor

Citation

Dierking, K, Polanowska, J, Omi, S, Engelmann, I, Gut, M, Lembo, F, Ewbank, JJ and Pujol, N (2011) Unusual regulation of a STAT protein by an SLC6 family transporter in C. elegans epidermal innate immunity. Cell Host Microbe 9:425-35

Abstract

The cuticle and epidermis of Caenorhabditis elegans provide the first line of defense against invading pathogens. Upon invasion by the fungal pathogen Drechmeria coniospora, C. elegans responds by upregulating the expression of antimicrobial peptides (AMPs) in the epidermis via activation of at least two pathways, a neuroendocrine TGF-β pathway and a p38 MAPK pathway. Here, we identify the sodium-neurotransmitter symporter SNF-12, a member of the solute carrier family (SLC6), as being essential for both these immune signaling pathways. We also identify the STAT transcription factor-like protein STA-2 as a direct physical interactor of SNF-12 and show that the two proteins function together to regulate AMP gene expression in the epidermis. Both SNF-12 and STA-2 act cell autonomously and specifically in the epidermis to govern the transcriptional response to fungal infection. These findings reveal an unorthodox mode of regulation for a STAT factor and highlight the molecular plasticity of innate immune signaling.

Links

PubMed Online version:10.1016/j.chom.2011.04.011

Keywords

Animals; Antimicrobial Cationic Peptides/biosynthesis; Caenorhabditis elegans/genetics; Caenorhabditis elegans/immunology; Caenorhabditis elegans Proteins/metabolism; Epidermis/immunology; GABA Plasma Membrane Transport Proteins/metabolism; Gene Expression Regulation; Hypocreales/immunology; Immunity, Innate; Models, Biological; Protein Binding; Protein Interaction Mapping; STAT Transcription Factors/metabolism

public



Cancel