A G184S point mutation was created in the Gnai2 (guanine nucleotide binding protein (G protein), alpha inhibiting 2; also called Gαi2) gene. A complex phenotype affecting multiple organ systems (heart, myeloid, skeletal, and central nervous system) can be observed. This strain may be useful in studies of signal transduction, pharmacology, diabetes, epilepsy, thrombosis, cardiology, and developmental biology.
Dr. Richard Neubig, Michigan State University
Genetic Background | Generation |
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Allele Type | Gene Symbol | Gene Name |
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Targeted (Not Applicable) | Gnai2 | guanine nucleotide binding protein (G protein), alpha inhibiting 2 |
A G184S point mutation was created in the Gnai2 (guanine nucleotide binding protein (G protein), alpha inhibiting 2; also called Gαi2) gene which disrupts interactions with regulator of G protein signaling (RGS) proteins that normally deactivate Gα G protein signals. A complex phenotype affecting multiple organ systems (heart, myeloid, skeletal, and central nervous system) can be observed. Homozygous mice and their cardiocytes exhibit enhanced muscarinic (M2) but not adenosine (A1) receptor-mediated responses. Isoproterenol-stimulated beating rates of heterozygous and homozygous hearts are significantly more sensitive to inhibition to carbachol than are those of wildtype mice.
Homozygous mice show slightly reduced adiposity. Unlike females, males placed on a high-fat diet are resistant to weight gain and have decreased body fat as compared to wildtype mice. Both males and females exhibit enhanced insulin sensitivity (protected from insulin resistance) and increased glucose tolerance.
Although fertile, both homozygotes and heterozygotes demonstrate reduced viability and decreased body weight. Homozygotes are born in low numbers for unknown reasons. Shortened long bones, growth retardation, enlarged spleen, elevated neutrophil and monocyte counts, enlarged heart, and behavioral hyperactivity are also observed primarily in homozygotes. This strain may be useful in studies of signal transduction, pharmacology, diabetes, epilepsy, thrombosis, cardiology, and developmental biology.
A G184S mutation was introduced to exon 5 and a loxP-flanked neomycin cassette was placed in intron 5 of the targeted gene using 129S1/Sv-Oca2pTyr+Kitl +-derived CJ7 embryonic stem (ES) cells. The floxed neomycin cassette was excised in resultant mice by crossing them with Zp3-cre mice on a C57BL/6 background (see Stock No. 003651). The strain was backcrossed to C57BL/6 for 15 generations by the donating laboratory.
Allele Name | targeted mutation 1.1, Richard R Neubig |
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Allele Type | Targeted (Not Applicable) |
Allele Synonym(s) | Galphai2G184S; Galphai2GS |
Gene Symbol and Name | Gnai2, guanine nucleotide binding protein (G protein), alpha inhibiting 2 |
Gene Synonym(s) | |
Promoter | Gnai2, guanine nucleotide binding protein (G protein), alpha inhibiting 2, mouse, laboratory |
Strain of Origin | 129S1/Sv-Oca2+ Tyr+ Kitl+ |
Chromosome | 9 |
Molecular Note | Cre mediated recombination resulted in the loss of the floxed neo from Gnai2tm1Rneu, leaving a glycine to serine substitution G184S in exon 5. |
Mutations Made By | Dr. Richard Neubig, Michigan State University |
When maintained as a live colony, heterozgyotes may be bred. Heterozygote x Heterozygote crosses reportedly produce 6-8% homozygous pups. Homozygote x Homozygote crosses are said to produce fewer, smaller litters (~4 pups per litter).
When using the B6.129S1-Gnai2tm1.1Rneu/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #012768 in your Materials and Methods section.
Facility Barrier Level Descriptions
Service/Product | Description | Price |
---|---|---|
Heterozygous or wildtype for Gnai2<tm1.1Rneu> |
Frozen Mouse Embryo | B6.129S1-Gnai2<tm1.1Rneu>/J Frozen Embryo | $2595.00 |
Frozen Mouse Embryo | B6.129S1-Gnai2<tm1.1Rneu>/J Frozen Embryo | $2595.00 |
Frozen Mouse Embryo | B6.129S1-Gnai2<tm1.1Rneu>/J Frozen Embryo | $3373.50 |
Frozen Mouse Embryo | B6.129S1-Gnai2<tm1.1Rneu>/J Frozen Embryo | $3373.50 |
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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.
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