Both heterozygous and homozygous Pkcp (Porkchop) mutant mice rapidly become obese without signs of diabetes.
Dr. Joseph S. Takahashi, Univ Texas Southwestern Medical Ctr
The semidominant porkchop (Pkcp) allele of the Mc4r (melanocortin 4 receptor) gene is defined by an arginine to tryoptophan (R147W; AGG->TGG) mutation.
By 60-80 days of age, both heterozygous and homozygous mice (males and females) are significantly heavier than wildtype littermates. Homozygotes develop the obese phenotype earlier and are more severely affected than the heterozygotes. Diabetes has not been observed. Obesity can interfere with the ability of homozygotes to effectively breed.
The semidominant Pkcp mutation in the Mc4r gene was created using ENU mutagenesis techniques by the Center for Functional Genomics (CFG) at Northwestern University as part of their Neurogenomics Project. Arginine 147 was mutated to tryptophan (R147W; AGG->TGG). The mutation was created and maintained on a C57BL/6J genetic background by the donating laboratory.
|Allele Name||pork chop|
|Allele Type||Chemically induced (ENU)|
|Gene Symbol and Name||Mc4r, melanocortin 4 receptor|
|Strain of Origin||C57BL/6J|
|Molecular Note||ENU mutagenesis induced an A to T point mutation that results in the amino acid substitution of tryptophan for arginine at position 147 (R147W).|
Heterozygotes and lean homozygotes are viable and fertile, but obese animals fail to reproduce effectively.
When using the Porkchop mouse strain in a publication, please cite the originating article(s) and include JAX stock #025249 in your Materials and Methods section.