Dbmc3^C57BL/6J
QTL Variant Detail

Summary

• QTL variant: Dbmc3^C57BL/6J
• Name: diabetes mRNA cluster 3; C57BL/6J
• MGI ID: MGI:3702986
• QTL: Dbmc3 Location: unknown Genetic Position: Chr9, Syntenic

Variant origin

• Strain of Specimen: C57BL/6J

Variant description

• Allele Type: QTL
• Mutation: Undefined
• Mutation details: This allele confers increased Scd1 liver mRNA expression with the insulin phenotype compared to BTBR. (J:119260)
• Inheritance: Dominant

Notes

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

J:119260

A genome wide scan was performed on 108 (BTBR x C57BL/6J) F2-ob/ob intercross animals, using 192 polymorphic markers, to identify loci affecting liver mRNA expression of 7 metabolic genes in correlation with diabetes traits. Male (BTBR x C57BL/6J) F1 hybrid animals develop severe hyperglycemia while neither parental strain exhibits diabetes or obesity phenotypes.

Linkage to Scd1, Fas, and Gpat expression with the insulin trait mapped to 66 cM on mouse Chromosome 2 near D2Mit106 (LOD=7.7). This locus spans approximately 60 cM - 90 cM and is named Dbmc1 (diabetes mRNA cluster 1). Scd1 expression accounts for the majority of the effect at Dbmc1, with BTBR-derived alleles conferring dominantly inherited increased Scd1 expression. T2dm3 is a previously identified insulin QTL mapping near Dbmc1.

Linkage to Scd1, Fas, and Gpat expression with the insulin trait mapped to 60 cM on mouse Chromosome 5 near D5Mit240 (LOD=4.5). This locus spans approximately 40 cM - 60 cM and is named Dbmc2 (diabetes mRNA cluster 2). Again, Scd1 expression accounts for the majority of the effect at Dbmc2, with BTBR-derived alleles conferring dominantly inherited increased Scd1 expression.

Dbmc3 (diabetes mRNA cluster 3) mapped to mouse Chromosome 9. C57BL/6J-derived alleles at Dbmc3 confer increased Scd1 expression with dominant inheritance.

References

• Original: J:119260 Lan H, et al., Dimension reduction for mapping mRNA abundance as quantitative traits. Genetics. 2003 Aug;164(4):1607-14
• All: 1 reference(s)