A conserved Toll-like receptor is required for Caenorhabditis elegans innate immunity.
Pathogen recognition through Toll-like receptors (TLRs) is crucial in order to mount an appropriate immune response against microorganisms. On the basis of a lack of evidence indicating that Caenorhabditis elegans uses TLRs to elicit an immune response and on the absence of genes encoding Rel-like transcription factors in its genome, it is believed that TLR-mediated immunity arose after coelomates split from pseudocoelomates and acoelomates. Here, we show that C. elegans tol-1(nr2033) mutants are killed by the human pathogen Salmonella enterica, which causes a significant pharyngeal invasion in the absence of TOL-1-mediated immunity. We also show that TOL-1 is required for the correct expression of ABF-2, which is a defensin-like molecule expressed in the pharynx, and heat-shock protein 16.41, which is also expressed in the pharynx and is part of a HSP family of proteins required for C. elegans immunity. The results indicate that TOL-1 has a direct role in defence response to certain Gram-negative bacteria and indicate that part of the TLR-mediated immunity might be evolutionarily conserved.
Tenor
Jennifer L
JL
Department of Molecular Genetics and Microbiology, Duke University Medical Center, Duke University, Durham, NC 27710, USA.
Aballay
Alejandro
A
D000818:Animals; D017173:Caenorhabditis elegans / Q000166:cytology / Q000276:immunology* / Q000382:microbiology; D029742:Caenorhabditis elegans Proteins / Q000276:immunology*; D017124:Conserved Sequence; D007113:Immunity, Innate / Q000276:immunology*; D009154:Mutation / Q000235:genetics; D009419:Nerve Tissue Proteins / Q000276:immunology*; D010614:Pharynx / Q000276:immunology / Q000382:microbiology; D019779:Salmonella enterica / Q000166:cytology
D029742:Caenorhabditis elegans Proteins; D009419:Nerve Tissue Proteins; C439300:Tol-1 protein, C elegans