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QTL Variant Detail
QTL variant: Char9C57BL/6J
Name: P. chabaudi malaria resistance QTL 9; C57BL/6J
MGI ID: MGI:3714005
QTL: Char9  Location: unknown  Genetic Position: Chr10, Syntenic
Strain of Specimen:  C57BL/6J
Allele Type:    QTL
Mutation:    Undefined
    This allele confers resistance to Plasmodium chabaudi infection compared to A/J. (J:122131)
Inheritance:    Codominant
View phenotypes and curated references for all genotypes (concatenated display).
Char9 has a stronger effect in males compared to females.

Mapping and Phenotype information for this QTL, its variants and associated markers


Recombinant congenic strain AcB55 is resistant to malaria and is derived from parental strains A/J (susceptible) and C57BL/6J (resistant). An F2 cross between AcB55 and A/J was analyzed for linkage to malaria resistance. PklrChar4 on mouse Chromosome 3controls 30% of the phenotypic variance. A suggestive locus near D10Mit189 (7 cM) on mouse Chromosome 10 was further analyzed while controlling for PklrChar4. This resulted in significant linkage to malaria resistance at 4 cM near D10Mit167 (LOD=4.57).This locus controls 8% of the variance and is designated Char9 (P. chabaudi malaria resistance QTL 9). C57BL/6J-derived alleles at Char9 confer codominant malaria resistance.

The Char9 locus spans 14 Mb and contains 77 genes. RT-PCR analysis of A/J andAcB55 mRNA revealed highly significant differential expression of Vnn3, with AcB55 expressing 12-fold more Vnn3 mRNA compared to A/J (p<0.0001).

SNP analysis revealed a 4 Mb haplotype block conserved among 5 out of 6 known malaria-susceptible strains (SJL/J, C3H/HeJ, BALB/cJ, AKR/J, and A/J). Vnn3 maps to this haplotype block and displays 100% correlation between genotype and transcript expression level. The A/J-derived Vnn3 transcript carries a C1592T nucleotide substitution resulting in premature stop codon and 7 amino acid truncation.

In addition, Vnn3 and Vnn1, a similar gene 30 Kb downstream from Vnn3, are present in liver mRNA from C57BL/6 and AcB55 resistant strains but are absent in liver mRNA from susceptible A/J and AcB61 strains. Analysis of the Vnn3 putative proximal promoter region revealed the A/J sequence contains complex rearrangements that could possibly explain the lack of transcriptional activity in this strain.

Original:  J:122131 Min-Oo G, et al., Complex genetic control of susceptibility to malaria: positional cloning of the Char9 locus. J Exp Med. 2007 Mar 19;204(3):511-24
All:  1 reference(s)

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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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