What question did this study set out to answer?

Determine the genetic basis of defective lipopolysaccharide signal transduction and endotoxin resistance in C3H/HeJ and C57BL/10ScCr mice.

December 11, 1998Science

Defective LPS Signaling in C3H/HeJ and C57BL/10ScCr Mice: Mutations in Tlr4 Gene

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Authors

APAlexander PoltorakBoston University XHXiaolong HeChinese Academy of Tropical Agricultural Sciences ISIrina SmirnovaTufts University

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Implication

Experimental genetic study reveals that Tlr4 mutations disrupt lipopolysaccharide signaling in mice, indicating a critical role for TLR4 in Gram-negative pathogen recognition.

Key Points

Determine the genetic basis of defective lipopolysaccharide signal transduction and endotoxin resistance in C3H/HeJ and C57BL/10ScCr mice.
Analyzed lipopolysaccharide signaling pathways and susceptibility to Gram-negative bacterial challenge in C3H/HeJ and C57BL/10ScCr mouse strains.
Identified and sequenced the Toll-like receptor-4 (Tlr4) gene corresponding to the Lps locus across mouse models.
Demonstrated that the codominant Lpsd allele in C3H/HeJ mice results from a missense mutation in exon 3 of Tlr4, substituting histidine for proline at position 712.
Identified a homozygous null mutation of Tlr4 in C57BL/10ScCr mice, confirming that disruption of Tlr4 selectively abolishes endotoxin signaling while predisposing mice to Gram-negative infection.

Cite This Study

Poltorak et al. (1998) studied this question.

synapsesocial.com/papers/6a017dcfbd6301933f5c9aee https://doi.org/10.1126/science.282.5396.2085

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Implication

Experimental genetic study reveals that Tlr4 mutations disrupt lipopolysaccharide signaling in mice, indicating a critical role for TLR4 in Gram-negative pathogen recognition.

Defective LPS Signaling in C3H/HeJ and C57BL/10ScCr Mice: Mutations in Tlr4 Gene

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Implication

Key Points

Cite This Study

Defective LPS Signaling in C3H/HeJ and C57BL/10ScCr Mice: Mutations in Tlr4 Gene

Discussion

Member takes

Implication

Key Points

Cite This Study

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