Newly Available JAX® Mice Strains
JAX® NOTES Issue 509, Spring 2008
Below is a partial list of newly available JAX® Mice strains. For a complete list, see Newly Available Strains.
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B6.Cg-Foxp3tm2Tch/J 006772
This strain has a targeted mutation of the forkhead fox P3 (Foxp3) gene. Homozygotes are viable, fertile, and develop normal T and B cells. They co-express Enhanced Green Fluorescent Protein (EGFP) and Foxp3 under the control of the endogenous promoter. EGFP expression accurately identifies the Foxp3+ T cell population (more than 97% of Foxp3+ T cells are EGFP+), and Foxp3 mRNA expression strictly segregates with EGFP+ T cells. Due to X-inactivation in females, the number of EGFP+CD4+ T cells in the peripheral blood of heterozygous females is approximately half that in hemizygous males. Following stimulation with anti-CD3 and anti-CD28 monclonal antibodies, suppression of effector cell proliferation by CD4+EGFP+ cells is normal. Some EGFP is expressed in a small population of CD8+ thymocytes. This strain may be used in immunological studies, including studies of regulatory T cell proliferation, localization, and antigen independence during the primary immune response.
B6.Cg-Tg(Cdh5-cre)7Mlia/J 006137
The construct in this transgenic strain includes Cre recombinase cDNA placed downstream of a 2.5-kb fragment of the VE-Cadherin (Cdh5) mouse promoter. Hemizygotes are viable, fertile, and look and behave normally. cre expression is observed as early as embryonic day 7.5 (E7.5) and progresses to nearly full penetrance in the differentiated endothelium by E14.5. In adult mice, cre is uniformly expressed in the endothelium of developing and quiescent vessels of all organs examined, and in a subset of hematopoietic cells. When bred with any mouse containing a loxP-flanked sequence of interest, offspring are produced in which Cre-mediated recombination deletes the flanked genome. This strain may be used to research the cardiovascular system (including angiogenesis) and endothelial and hematopoietic cell lineages.
B6.Cg-Tg(Thy1-COP4/EYFP)18Gfng/J 007612
These founder line 18 transgenic mice express the light-activated ion channel, Channelrhodopsin-2 (from the green alga Chlamydomonas reinhardtii), fused to yellow fluorescent protein (ChR2-YFP) under the control of the mouse thymus cell antigen 1 (Thy1) promoter. Hemizygotes are viable, fertile, and look and behave normally. Expression of the transgenic ChR2-YFP fusion protein is detected in layer 5 cortical neurons, CA1 and CA3 pyramidal neurons of the hippocampus, cerebellar mossy fibers, neurons in the thalamus, midbrain and brainstem, and the olfactory bulb mitral cells. Neurons expressing the transgene are morphologically and physiologically comparable to non-mutant neurons. This mutant mouse strain may be useful for ex vivo and in vivo neural circuitry mapping studies using light stimulation.
B6.Cg-Ikbketm1Tman/J 006908
Homozygotes for this targeted mutation of the inhibitor of kappaB kinase epsilon (Ikbke) gene are viable and fertile. There is no endogenous kinase function in the lungs, spleen, and embryonic fibroblasts. Due to defective inteferon (IFN) signaling, these mice have increased susceptibility to viral infection. They may be used in immunological studies involving IFN signaling and host responses to infection.
B6;CB-Tg(Thy1-CFP/COX8A)S2Lich/J 006617
These transgenic mice express cyan fluorescent protein (CFP) under the control of the mouse thymus cell antigen 1, theta (Thy1) gene promoter. Homozygotes are viable, fertile, and look and behave normally. CFP is specifically localized to the mitochondria by a human cytochrome c oxidase, subunit 8A (ubiquitous), targeting signal fused to the N-terminus. Fluorescence is detected in many neuronal populations, including retinal ganglion cells, bipolar cells, amacrine cells, and photoreceptors. Neuronal, mitochondrial, and neuromuscular junction morphology appears normal. Axonal mitochondrial density is similar to that in wild-type mice. This strain may be used to research mitochondrial transport in adult motor neurons.
FVB-Tg(Nr5a1-cre)2Lowl/J 006364
Mice hemizygous for this nuclear receptor subfamily 5, group A, member 1 (Nr5a1), or steroidogenic factor-1-Cre (Sf1-Cre), transgene are viable, fertile, and look and behave normally. Transgene expression mimics the Nr5a1 mRNA pattern with Cre activity observed in SF1-positive neurons in the ventromedial hypothalamic nucleus (VMH), pituitary, gonads, and adrenals. Expression is also noted in the cerebral cortex and in a few scattered cells in the caudal brainstem of mice derived from line 2 (but not line 7). If this strain is bred with one containing a loxP-flanked sequence of interest, offspring are produced in which tissue-specific deletion of the transgene results. This strain may be used to research the hypothalamus (body weight homeostasis, obesity, leptin metabolism, etc) or as a reporter strain for SF1-transcription factor activity.
B6.129P2(C)-Cd19tm1(cre)Cgn/J 006785
In this strain, a Cre cassette is inserted into exon 2 of and functionally disrupts the CD19 antigen (Cd19) gene. The Cd19 promoter specifically directs expression at the earliest stages and throughout B-lymphocyte development and differentiation. Homozygotes are viable, fertile, and look and behave normally. However, they are deficient in the B-1 subset of B-lymphocytes, have low serum IgM levels, have a severely impaired ability to respond to T-cell-dependent antigens, and fail to form splenic germinal centers. Heterozygotes are phenotypically normal and can be used to delete floxed targets in B-lymphocytes.
B6.129P2(C)-Ccr7tm1Rfor/J 006621
Homozygotes for this targeted mutation of the chemokine (C-C motif) receptor 7 (Ccr7) gene are viable, fertile, but have delayed primary B or T cell immune responses. Although, lymph nodes from homozygotes are devoid of naive T cells and dendritic cells, the T cell population is heavily expanded in the blood, the red pulp of the spleen, and the bone marrow. Secondary lymph organs are morphologically abnormal, and adoptive transfer experiments demonstrate impaired B- and T-cell migration. In a model of acute allogeneic tumor rejection, homozygotes fail to reject subcutaneously injected MHC class I mismatched tumor cells, and cytotoxic activity of allospecific T cells is severely compromised. This strain (along with B6.129S2(Cg)-Cxcr5tm1Lipp/J, 006659) may be used to research chemokine receptors, such as studies of T- and B-cell function in primary and adaptive immune responses, entry of lymphocytes and dendritic cells into secondary lymphoid organs (and their homing to T- and B-cell zones therein), alloimmune responses, and development of transplant rejection.
B6.129S2(Cg)-Cxcr5tm1Lipp/J 006659
Homozygotes for this targeted mutation of the chemochine (C-X-C motif) receptor 5 (Cxcr5) gene are viable and fertile. Multiple lymphoid organs lack detectable levels of targeted protein, and RNA transcripts are also absent in spleen cells. Homozygotes have a complex pattern of lymph node and PeyerÕs patches defects. In addition, they have a completely disorganized splenic microarchitecture, lacking segregated T- and B-cell areas within the splenic white pulp. This strain (along with B6.129P2(C)-Ccr7tm1Rfor/J, 006621) may be used in immunological studies of chemokine receptors, such as studies of T- and B-cell function in primary and adaptive immune responses, entry of lymphocytes and dendritic cells into secondary lymphoid organs and their homing to T- and B-cell zones therein.
B6.129S6-Per2tm1Jt/J 006852
Homozygotes for this targeted mutation of the Drosophila period homolog 2 (Per2) gene are viable, and look normal. The expression of PERIOD2::LUCIFERASE (or mPER2::LUC) fusion protein during peak periods is similar to that of endogenous pPER2 expression. Homozygotes have normal entrainment and circadian behaviors. This strain may be used as real-time reporter of circadian dynamics in different tissues.
STOCK Tg(ACTB-Bgeo,-NOTCH1,-EGFP)1Lbe/J 006850
Hemizygotes for this Cre-conditional IC-Notch (or Z/EG-Notch) transgene are viable and fertile. Homozygotes die in utero, presumably from high lacZ expression. Before Cre-mediated excision of the "floxed" STOP sequence, lacZ is highly expressed. When this strain is bred to one expressing Cre recombinase, offspring are produced in which the STOP sequence (and beta-geo) is removed, allowing the Cre recombinase-expressing cells to transcribe and co-express both the intracellular human NOTCH1 (IC-Notch) and EGFP. For example, various cre-transgenic matings that result in endothelial expression of IC-Notch produce offspring with neural, somite, and angiogenic defects, infertile females, or that die in utero. These transgenic mice may be useful for global expression of lacZ or for studying the role of Notch signaling during both embryonic development and adulthood.
FVB.BKS(D)-Leprdb/ChuaJ 006654
The phenotype of this congenic "FVB-db" strain varies from that on other genetic backgrounds. Specifically, whereas the hyperglycemia of C57BLKS/J-db mice is due to the development of hypoinsulinemia and loss of beta-cell mass, the hyperglycemia of this strain appears to be due to severe insulin resistance along and continual increases in insulin secretory capacity from beta-cell mass expansion. The hyperglycemia in the fed state persists despite escalating insulin secretion and massive increase of pancreatic beta-cells. These mice show evidence of mesangial matrix expansion, a hallmark of diabetic nephropathy. This strain, along with db mutants on other genetic backgrounds (see Stock Numbers 000642, 000697, 000699, 000700, and 000707), may be used to research diabetes, including the genetic control of beta-cell responses to hyperglycemia and insulin resistance/sensitivity.
B6.129S4-Park2tm1Shn/J 006582
Homozygotes for this targeted mutation of the parkin (Park2) gene are viable and fertile, but brain morphology is grossly normal. Western blot analysis using antibody specific to C-terminal sequences indicates the absence of full length gene product. RT-PCR shows that exon 2 splices to exon 4, skipping exon 3 entirely, resulting in a frame shift and a premature stop codon in exon 5. Whereas EGFP transcripts are present, little parkin-EGFP fusion protein is detectable by Western analysis. Homozygotes have increased extracellular dopamine concentration in the striatum. Further, medium-sized striatal spiny neurons require greater currents to induce synaptic responses, suggesting a reduction in synaptic excitability in the absence of the endogenous gene. Homozygotes also exhibit deficits in behavioral paradigms sensitive to dysfunction of the nigrostriatal pathway. However, compared to the substantial loss of nigral neurons characteristic of Parkinson's disease, the numbers of dopaminergic neurons in the substantia nigra are normal up to the age of 24 months. Homozygotes and their isolated cells exhibit mitochondrial dysfunction and impaired protection from oxidative stress. Muscle cells isolated from homozygotes have defective skeletal muscle mitochondrial homeostasis and increased sensitivity to amyloid-beta toxicity. This strain models the exon 3 deletion mutation most common in human autosomal recessive juvenile parkinsonism (AR-JP) patients and may be used to research Parkinson's disease, dopamine regulation, nigrostriatal function, mitochondrial function, and other neurobiological research.
STOCK Tg(Olfr16,taulacZ)2030Mom/MomJ 006674
Hemizygous mice express a mini-transgene for the olfactory receptor MOR23. Olfactory sensory neurons that express MOR23 co-express the taulacZ fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. This strain may be to research axon guidance and mechanisms of olfactory receptor specificity in the olfactory bulb.
