Abstract
The Toll-dependent defense against Gram-positive bacterial infections in Drosophila is mediated through the peptidoglycan recognition protein SA (PGRP-SA). A mutation termed osiris disrupts the Gram-negative binding protein 1 (GNBP1) gene and leads to compromised survival of mutant flies after Gram-positive infections, but not after fungal or Gram-negative bacterial challenge. Our results demonstrate that GNBP1 and PGRP-SA can jointly activate the Toll pathway. The potential for a combination of distinct proteins to mediate detection of infectious nonself in the fly will refine the concept of pattern recognition in insects.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Carrier Proteins / genetics
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Carrier Proteins / metabolism*
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DNA Transposable Elements
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Drosophila / genetics
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Drosophila / immunology
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Drosophila / metabolism*
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Drosophila / microbiology*
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Drosophila Proteins / genetics
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Drosophila Proteins / metabolism*
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Gene Expression
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Genes, Insect
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Gram-Negative Bacteria / physiology*
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Gram-Positive Bacteria / physiology*
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Hemolymph / metabolism
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Hypocreales / physiology
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Insect Proteins / genetics
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Insect Proteins / metabolism
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Mutation
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Phenotype
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Receptors, Cell Surface / genetics
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Receptors, Cell Surface / metabolism*
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Serine Endopeptidases / genetics
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Serine Endopeptidases / metabolism
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Toll-Like Receptors
Substances
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Carrier Proteins
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DNA Transposable Elements
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DptA protein, Drosophila
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Drosophila Proteins
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Gnbp1 protein, Drosophila
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Insect Proteins
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Receptors, Cell Surface
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Tl protein, Drosophila
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Toll-Like Receptors
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peptidoglycan recognition protein
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spz protein, Drosophila
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DRS protein, Drosophila
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Serine Endopeptidases
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psh protein, Drosophila