Summary |
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Variant origin |
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Variant description |
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Phenotypes |
View phenotypes and curated references for all genotypes (concatenated display).
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Notes |
Why1 and Why2 engage in epistatic interactions.
Mapping and Phenotype information for this QTL, its variants and associated markersJ:131437Linkage analysis was performed on 82 C57BL/6J x (C57BL/6J x MOLF/EiJ)F1 backcross animals to identify QTLs associated with Toll-like receptor (TLR) mediated cytokine production. IL-6 production after stimulation of macrophages with lipoteichoic acid (LTA) was assessed as a measure of TLR-mediated cytokine responsiveness. Significant linkage to cytokine response mapped to 49 cM on mouse Chromosome 6 near D6Mit328 (LOD=3.69). This locus is named Why1 (wild-derived hyperresponse 1). The MOLF/EiJ-derived allele confersincreased IL-6 production (cytokine response) after LTA stimulation. Irak2 (49.5 cM) is a potential candidate gene for Why1. Several polymorphisms exist between the Irak2 gene sequences of C57BL/6J and MOLF/EiJ. However, these polymorphisms do not appearto correlate with the phenotype. Why2 (wild-derived hyperresponse 2) mapped to 41 cM on mouse Chromosome 9 near D9Mit155 (LOD=5.49). This locus appears to act negatively with MOLF/EiJ-derived alleles conferring decreased IL-6 production. The QTL interval spans 23 cM. Microarray analysis identified Irak1bp1 as a potential candidate gene displaying 20-fold expression difference between C57BL/6J and MOLF/EiJ. Northern blot analysis showed increased Irak1bp1 expression in MOLF/EiJ macrophages after LTA stimulation compared to C57BL/6J macrophages. Why1 (chr6) and Why2 (chr9) exhibit significant epistatic interaction (LRS=48.1). Authors hypothesize Why2 evolved as a negative regulator of the pro-inflammatory effects of Why1. |
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References |
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 11/12/2024 MGI 6.24 |
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