In this strain, exon 4 of the endogenous neuropeptide S receptor 1 (Npsr1 or GPRA) gene is replaced with a neo cassette, abolishing ligand binding function. These GPRA mutant mice may be useful for studying the induction of asthma-like disease, smooth muscle constriction, and airway function.
Beverly H Koller, University of North Carolina at Chapel Hill
In this strain, exon 4 of the endogenous neuropeptide S receptor 1 (Npsr1 or GPRA) gene is replaced with a neo cassette, abolishing ligand binding function. Homozygous (GPRA-/-) mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. GPRA-/- mice on a 129/SvEv genetic background show an attenuated response when challenged with the cholinergic receptor-dependent bronchoconstricting agent thromboxane. These GPRA mutant mice may be useful for studying the induction of asthma-like disease, smooth muscle constriction, and airway function.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
A targeting vector was designed to replace exons 4 encoding the neuropeptide S receptor 1 (Npsr1 or G protein-coupled receptor for asthma susceptibility,Gpra) gene with a neomycin resistance (neo) cassette. The construct was electroporated into 129S6/SvEvTac-derived TC1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into blastocysts and the resulting chimeric males were bred to B6D2 females and subsequently to BALB/C mice to generate a colony of Gpra-/- mice. The donating investigator reports that these mice were backcrossed at least 12 generations to C57BL/6 background (see SNP note below). Upon arrival at The Jackson Laboratory, mice were bred to C57BL/6J (Stock No. 000664) for at least one generation to establish the colony.
A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, at least 1 of 5 markers that determine C57BL/6J from C57BL/6N were found to be segregating. These data suggest the mice sent to The Jackson Laboratory Repository were on a mixed C57BL/6J ; C57BL/6N genetic background.
|Allele Name||targeted mutation 1, Beverly H Koller|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Npsr1, neuropeptide S receptor 1|
|Strain of Origin||129S6/SvEvTac|
|Molecular Note||Exon 4 was replaced with a neo cassette. Northern blot analysis confirmed the expression of a truncated transcript.|
|Mutations Made By|| |
Beverly Koller, University of North Carolina at Chapel Hill
When maintaining a live colony, homozygous mice may be bred together.
When using the B6.129S6(Cg)-Npsr1tm1Bhk/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #013245 in your Materials and Methods section.