Bglu3^C3H/HeJ
QTL Variant Detail

Summary

• QTL variant: Bglu3^C3H/HeJ
• Name: blood glucose level 3; C3H/HeJ
• MGI ID: MGI:3624637
• QTL: Bglu3 Location: Chr1:172831765-172831892 bp Genetic Position: Chr1, Syntenic

Variant origin

• Strain of Specimen: C3H/HeJ

Variant description

• Allele Type: QTL
• Mutation: Undefined
• This allele confers increased plasma glucose levels and body weight compared to C57BL/6J. (J:108422)
• Inheritance: Dominant

Expression

In Mice Carrying this Mutation:	1 RNA-Seq or microarray experiment(s)
In Structures Affected by this Mutation:	2 anatomical structure(s)

Notes

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

J:108422

Loci linked to body weight, serum amyloid P (SAP), and hyperglycemia were mapped using 234 female animals from a (C57BL/6J-Apoe^tm1Unc x C3H/HeJ-Apoe^tm1Unc)F2 intercross. 134 polymorphic markers at an average resolution of 12 cM were used for the genome scan. Parental strain C3H/HeJ-Apoe^tm1Unc exhibit significantly increased body weight and plasma total cholesterol, HDL, and triglycerides, and slightly higher plasma glucose and insulin, compared to parental strain C57BL/6J-Apoe^tm1Unc.

A locus at95.8 cM (D1Mit206) on mouse Chromosome 1 named Bglu3 (blood glucose level 3) showed significant linkage to body weight (LOD=8.3), plasma glucose levels (LOD=4.1), and SAP (LOD=9.2). The Bglu3 support interval (SI) spans approximately 86 cM - 104 cM. C3H/HeJ-derived alleles at Bglu3 confer increased body weight and plasma glucose levels with a dominant mode of inheritance, and increased SAP with an additive mode of inheritance. Bglu3 explains 22% of the variance in glucose levels, 34% of the variance in body weight, and 66% of the variance in SAP. Apoa2 (92.6 cM) and Apcs (formerly Sap, 94.2 cM) map to the Bglu3 interval and are considered potential candidates. Previously identified body weight QTL Bw8q1 (100 cM) maps near Bglu3.

A second locus on mouse Chromosome 1 shows significant linkage to body weight at 81.6 cM (LOD=9 near D1Mit425). This locus explains 40% of the variance and is named Bodwt1 (body weight 1). The support interval for Bodwt1 spans 72 cM - 87 cM. C3H/HeJ-derived alleles at Bodwt1 confer increased body weight with a dominant mode of inheritance. A previously identified body weight QTL named Bw17 (69 cM) maps near this locus. A potential candidate gene mapping near Bodwt1 is Myog at 72.3 cM.

Significant linkage to body weight mapped to29.4 cM on mouse Chromosome 17 near D17Mit180 (LOD=3.4). This locus explains 7% of the variance and is named Bodwt2 (body weight 2). The support interval for Bodwt2 spans 19 cM - 35 cM. C3H/HeJ-derived alleles at Bodwt2 confer increased body weight with adominant mode of inheritance. A previously identified body weight QTL named Wt3q3 maps near this locus. Pla2g7 is a potential candidate gene for Bodwt2.

Suggestive loci for bodyweight mapped to 46 cM on mouse Chromosome 4 (LOD=2.7 at D4Mit153) and 54 cMon mouse Chromosome 14 (LOD=2.2 at D14Mit185). Suggestive linkage to plasma insulin mapped to 33 cM on mouse Chromosome 9 (LOD=2.7 at D9Mit207). Suggestive linkage to plasma glucose mapped to 38 cM on mouse Chromosome 9 (LOD=2.3 at D9Mit260).

References

• Original: J:108422 Su Z, et al., Genetic linkage of hyperglycemia, body weight and serum amyloid-P in an intercross between C57BL/6 and C3H apolipoprotein E-deficient mice. Hum Mol Genet. 2006 May 15;15(10):1650-8
• All: 1 reference(s)