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• W2107804596 abstract "Insects defend themselves against infectious microorganisms by synthesizing potent antimicrobial peptides. Drosophila has appeared in recent years as a favorable model to study this innate host defense. A genetic analysis of the regulation of the antifungal peptide drosomycin has demonstrated a key role for the transmembrane receptor Toll, which prompted the search for mammalian homologs. Two of these, Toll-like receptor (TLR)2 and TLR4, recently were shown to play a critical role in innate immunity against bacteria. Here we describe six additional Toll- related genes ( Toll-3 to Toll-8 ) in Drosophila in addition to 18-wheeler . Two of these genes, Toll-3 and Toll-4 , are expressed at a low level. Toll-6 , -7 , and -8 , on the other hand, are expressed at high levels during embryogenesis and molting, suggesting that, like Toll and 18w , they perform developmental functions. Finally, Toll-5 is expressed only in larvae and adults. By using chimeric constructs, we have tested the capacity of the signaling Toll/IL-1R homology domains of these receptors to activate antimicrobial peptide promoters and found that only Toll and Toll-5 can activate the drosomycin promoter in transfected cells, thus demonstrating specificity at the level of the Toll/IL-1R homology domain. In contrast, none of these constructs activated antibacterial peptide promoters, suggesting that Toll-related receptors are not involved in the regulation of antibacterial peptide expression. This result was independently confirmed by the demonstration that a dominant-negative version of the kinase Pelle can block induction of drosomycin by the cytokine Spaetzle, but does not affect induction of the antibacterial peptide attacin by lipopolysaccharide." @default.
• W2107804596 created "2016-06-24" @default.
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• W2107804596 date "2000-09-05" @default.
• W2107804596 modified "2023-10-03" @default.
• W2107804596 title "Toll-related receptors and the control of antimicrobial peptide expression in <i>Drosophila</i>" @default.
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• W2107804596 doi "https://doi.org/10.1073/pnas.180130797" @default.
• W2107804596 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/27057" @default.
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