These Lepr (leptin receptor) mutant mice carry a knockout allele derived from the targeted deletion of exon 1. Heterozygotes are phenotypically normal, viable, and fertile. Homozygotes are morbidly obese, infertile and resemble Leprdb-3J homozygous animals (also null for all Lepr isoforms). Plasma levels of leptin, glucose, insulin and corticosterone are elevated. Reported weights of males and females reach approximately 60g by 16 weeks of age.
A single loxP site was inserted 5' of exon 1 and a loxP-flanked neomycin and thymidine kinase selection cassette was inserted 3' of exon 1 using 129P2/OlaHsd-derived E14.1 embryonic stem (ES) cells. The floxed neomycin cassette was removed by transient Cre expression in the ES cells, leaving exon 1 flanked by loxP sites (see Stock No. 008327). Resultant mice were crossed with animals carrying an EIIa-cre to excise exon 1. This strain was backcrossed more than 10 times to C57BL/6J by the donating laboratory.
|Allele Name||targeted mutation 1.1, Jeffrey M Friedman|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Lepr, leptin receptor|
|Strain of Origin||129P2/OlaHsd|
|Molecular Note||This allele is a derivative of Leprtm1.1Rck in which exon 1 and flanking sequences were deleted in the germline by crossing mice carrying this allele to mice carrying Tg(EIIa-Cre)1Lmgd.|
Heterozygous mice may be bred to maintain a colony. Homozygotes are infertile due to a loss of leptin signaling.
When using the B6.129P2(Cg)-Leprtm1.1Rck/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #019377 in your Materials and Methods section.