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Variant origin |
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Variant description |
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Notes |
Mapping and Phenotype information for this QTL, its variants and associated markersJ:133125Linkage analysis was performed on 115 (C57BL/6J x BALB/cJ)F2 animals to identify QTLs associated with liver stage malaria resistance. Parental strain BALB/cJ displays decreased parasitemia 5 days after infection with Plasmodium berghei compared to parental strain C57BL/6J. It is believed resistance to malaria is due to reduced parasite expansion in the early liver stage. F2 animals were genotyped for 93 polymorphic markers and phenotyped for the presence of P.berghei 18S rRNA in the liver 40 hours after infection. Significant linkage to P.berghei resistance mapped to 34 cM on mouse Chromosome 17 near D17Mit20 (LOD=4.2). This locus explains 15.4% of the phenotypic variance and is named Belr1 (berghei liver resistance 1). A congenic line, B6.C-H2d/bByJ,carrying 38 Mb of BALB/cJ-derived DNA from D17Mit228 (16.4 cM) to D17Mit152 (37.7 cM) (encompassing the H2 locus) on a C57BL/6J genetic background confirmed Belr1. These animals display decreased parasite burden in the liver. However, the reciprocal congenic line C.B10-H2d/LilMcdJ does not display malaria susceptibility as would be expected. These congenic animals carry a smaller segment of C57BL/10-derived DNA from D17Mit228 (16.4 cM) to D17Mit24 (20.4 cM). Therefore, authors theorize Belr1 maps distal to the H2 locus. It is also possible genes within the H2 locus interact with Belr1 to modify the resistance phenotype. Char7 (34 cM) is a previously identified malaria susceptibility loci mapping near Belr1.Suggestive linkage to P.bergheiresistance mapped to distal mouse Chromosome 1 (LOD=2.73). This locus overlaps with previously identified cerebral malaria QTL Berr1 at 102 cM. |
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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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