Allele Symbol
Stock Number
Strain Name
Aw-J 001809On Hold
B6-Aw-J .Cg-EdaTa-6J +/+ ArTfm /J
Strain Description Testicular feminization (ArTfm ) is a dominant spontaneous mutation on the X chromosome. Hemizygous male mice are outwardly female in appearance except that the vagina does not open until 3 months of age if at all. Male reproductive development is abnormal leading to very small testes, and the absense of vas deferens, the epididymis, and male accessory glands. Spermatogonia and Sertoli cells are present in the testes, but spermatogenesis does not proceed past meiotic prophase. Leydig cells, which normally produce androgen in males, fail to develop normally. This strain is also segregating for the tabby 6J mutation (EdaTa-6J ) that affects both the coat color and hair pattern growth. The tabby mutation is maintained in repulsion with the testicular feminization mutation and is used as a coat color marker to assist in identifying resulting genotypes obtained from matings.
Aw-J 000314On Hold
B6CBACa Aw-J /A-EdaTa /J-XO
Strain Description
Aw-J 002703On Hold
B6CBACa Aw-J /A -Hydinhy3 /J
Strain Description Mice homozygous for the hydrocephalus 3 spontaneous mutation (Hydinhy3 ) are usually identifiable at 3 to 5 days. Those with frank hydrocephalus die by 4 or 5 weeks of age. The lateral ventricles and the third ventricle are enlarged, the aqueduct of Sylvius and the fourth ventricle are only slightly affected, and there is some dilatation of the ventral subarachnoid cistern. The hydrocephalus seems to be due to a defect in the subarachnoid space under the calvarium caused by an abnormal postnatal differentiation of the arachnoid mater and pia mater which prevents their separation. Penetrance is incomplete.
Adam2tm1Dgm 008042Under Development for Production
B6;129P2-Adam2tm1Dgm /J
Strain Description Mice homozygous for this fertilin b (Adam2 ) mutant allele are viable with no gross phenotypic abnormalities reported. Both precursor and processed fertilin b proteins were absent from spermatogenic cells and mature sperm isolated from homozygous males. While homozygous females are fertile with normal egg activation, homozygous males exhibit sperm deficiencies in sperm-egg membrane adhesion, sperm-egg fusion, migration from the uterus into the oviduct, and binding to the egg zona pellucida, rendering them infertile. These fertilin b (Adam2 ) mutant mice may be useful in reproductive biology studies; specifically to determine the role of ADAM (A Disintegrin And Metalloprotease) family proteins in sperm-egg interactions, fertilization, and spermatogenesis. These mice may also be useful in conjunction with other ADAM family mutant mice, including the cyritestin (Adam3 )-deficient strain (see Stock No. 008043 ).
Adam3tm1Pmkf 008043Under Development for Production
B6;129P2-Adam3tm1Pmkf /J
Strain Description Mice homozygous for this cyritestin (Adam3 ) mutant allele are viable with no gross phenotypic abnormalities reported. No protein product is detected from the targeted gene in sperm isolated from homozygous males. While homozygous females are fertile, homozygous males exhibit sperm deficiencies in adhesion to the egg zona pellucida and to the egg plasma membrane rendering them infertile. These cyritestin (Adam3 ) mutant mice may be useful in reproductive biology studies; specifically to determine the role of ADAM (A Disintegrin And Metalloprotease) family proteins in sperm-egg interactions, fertilization, and spermatogenesis. These mice may also be useful in conjunction with other ADAM family mutant mice, including the fertilin b (Adam2 )-deficient strain (see Stock No. 008042 ).
Adipoqtm1Chan 008195Under Development for Production
B6.129-Adipoqtm1Chan /J
Strain Description Homozygous mice are viable and fertile, with absence of targeted allele expression confirmed in adipose tissue (mRNA) and plasma (adiponectin protein). While homozygous mice have normal glucose tolerance and insulin resistance, beta-oxidation activity is significantly increased in muscle and liver. Homozygotes also have endothelial dysfunction (increased leukocyte rolling and leukocyte adhesion), are protected from DSS-induced colitis, and are more susceptible to myocardial ischemia/reperfusion. When fed a high fat diet, obese homozygotes are significantly heavier with increased insulin levels and altered insulin resistance. These adiponectin-deficient (Adipoq -/- or Adipo -/- ) mice may be useful in studying obesity, diabetes, insulin resistance, metabolism, inflammation, leukocyte-endothelium interactions, and colitis.
Akap6tm1Jsco 007447Under Development for Cryo
B6.129-Akap6tm1Jsco /14J
Strain Description Homozygous mice have reduced viability, especially on a C57BL/6 background. Approximately 1 out of 4 homozygotes are very small and die before reaching 2 weeks of age. The remaining homozygotes are 20-30% smaller than wildtype and heterozygous littermates; these survive and eventually become similar in size to wildtypes. All homozygotes have a characteristic craniofacial defect that includes a very pointed nose, eyes that are delayed in opening, and a shortened jaw. The alpha transcript of the gene is absent, as determined by brain mRNA and protein assays. Beta transcript RNA is present in heart and brain.
Akt2tm1.1Mbb 006952Under Development for Production
B6.Cg-Akt2tm1.1Mbb Ldlrtm1Her /J
Strain Description Independently, homozygous Akt2 mutant mice develop insulin resistance and diabetes, while LDLR homozygotes are predisposed to atherosclerosis. Double mutant mice that are heterozygous for the Akt2 allele and homozygous for the LDLR mutation are viable and fertile. These double mutant mice may be useful in studies of diabetes, metabolism, hyperglycemia, and atherosclerosis.
ArTfm 001809On Hold
B6-Aw-J .Cg-EdaTa-6J +/+ ArTfm /J
Strain Description Testicular feminization (ArTfm ) is a dominant spontaneous mutation on the X chromosome. Hemizygous male mice are outwardly female in appearance except that the vagina does not open until 3 months of age if at all. Male reproductive development is abnormal leading to very small testes, and the absense of vas deferens, the epididymis, and male accessory glands. Spermatogonia and Sertoli cells are present in the testes, but spermatogenesis does not proceed past meiotic prophase. Leydig cells, which normally produce androgen in males, fail to develop normally. This strain is also segregating for the tabby 6J mutation (EdaTa-6J ) that affects both the coat color and hair pattern growth. The tabby mutation is maintained in repulsion with the testicular feminization mutation and is used as a coat color marker to assist in identifying resulting genotypes obtained from matings.
Art2atm1Fkn 008252Under Development for Production
NOD.129S4(B6)-Art2atm1Fkn Art2btm1Fkn /LtJ
Strain Description Art2a, Art2b , commonly referred to as ART2, deficient mice are viable and fertile and do not show any overt phenotype. RT-PCR and FACS analysis confirm the absence of ART2 expression on the cell surface of thymic and lymph node purified T cells. No detectable histological abnormalities were observed in the thymus, spleens, lymph nodes, Peyer's patches, thyroid, brain, lung, kidney, intestine, liver, pancreas and thyroid. The disrupted introgression of ART2 onto the NOD background resulted in no significant difference in diabetes onset or incidence when compared to NOD. When the Cd38 targeted mutation is introduced to the NOD.ART2 deficient stock, the NOD.CD38, ART2 deficient males and females are completely resistant to diabetes. This is a surprising result as the NOD.CD38 deficient stock experiences accelerated diabetes onset and incidence in both males and females. Cd4 + and CD8 + T cells from ART2 deficient NOD mice are completely resistant to NAD induced apoptosis at all concentrations in vitro.
The ART2 targeted mutation provides a tool to further dissect the interplay of ADP rybosylation and NAD-catabolizing enzymes and their effect on Tregs and iNKT involved in autoimmune diseases specifically, Type 1 Diabetes.
Art2btm1Fkn 008252Under Development for Production
NOD.129S4(B6)-Art2atm1Fkn Art2btm1Fkn /LtJ
Strain Description Art2a, Art2b , commonly referred to as ART2, deficient mice are viable and fertile and do not show any overt phenotype. RT-PCR and FACS analysis confirm the absence of ART2 expression on the cell surface of thymic and lymph node purified T cells. No detectable histological abnormalities were observed in the thymus, spleens, lymph nodes, Peyer's patches, thyroid, brain, lung, kidney, intestine, liver, pancreas and thyroid. The disrupted introgression of ART2 onto the NOD background resulted in no significant difference in diabetes onset or incidence when compared to NOD. When the Cd38 targeted mutation is introduced to the NOD.ART2 deficient stock, the NOD.CD38, ART2 deficient males and females are completely resistant to diabetes. This is a surprising result as the NOD.CD38 deficient stock experiences accelerated diabetes onset and incidence in both males and females. Cd4 + and CD8 + T cells from ART2 deficient NOD mice are completely resistant to NAD induced apoptosis at all concentrations in vitro.
The ART2 targeted mutation provides a tool to further dissect the interplay of ADP rybosylation and NAD-catabolizing enzymes and their effect on Tregs and iNKT involved in autoimmune diseases specifically, Type 1 Diabetes.
Atcayji 008140Under Development for Production
B6.C(Cg)-Atcayji /BurJ
Strain Description ji homozygotes can first be identified at approximately 12 days of age by a leaning, zig-zag gait when they attempt to run and by the difficulty they have righting themselves when placed on their backs. Disease progression is rapid such that within two more days mutants are found to crouch on their heels in a squatting position and can not run without falling. Within three to four days of the first symptoms, tetany is seen during exertion or excitement. This is initially most pronounced in the forelegs, which the mice beat up and down during these two- to three-second spasms. Failure to gain weight is seen by the third week of life and it is unclear whether this results from an inability to take in food. The severity and frequency of tetany increases, and during the fourth week weight loss and increased weakness precede death. The mean age of death is approximately 31 days. Tetrahydrobiopterin levels in the brain and GTP cyclohydrolase activity in the liver are lower in ji homozygotes than normal. At 20 days of age, serum calcium is within normal ranges. Parabiotic twins made with an affected and an unaffected sibling do not transfer a mutant phenotype to the normal partner indicating that a diffusible factor does not cause the mutant phenotype. However, tetany and weight loss are inhibited in the mutant partner which also has increased longevity, yet still develops failed muscle coordination and a crouching posture. (DeOme, 1945; Snell, 1950; Duch et al., 1986.)
B4galt1tm1Shur 006941Under Development for Production
B6.129S7-B4galt1tm1Shur /J
Strain Description Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Ninety percent of homozygotes die soon after birth or within 2-3 weeks of birth. Surviving homozygotes are initially smaller than wildtype or heterozygotes and exhibit abnormal skin and coat, but assume a normal growth rate and appearance at 3 to 4 weeks of age. No gene product (mRNA) is detected by RT-PCR analysis of homozygous tissues. Neither the long or short isoform is expressed. Beta 1,4-galactosyltransferase enzyme activity is undetectable except for residual activity in brain and testis. Galactose residues are absent from testis. Heterozygotes have an intermediate enzyme activity level. Surviving homozygotes exhibit puffy faces (hypothyroid myxedema), thin skin, decreased density of hair follicles, reduction in subdermal adipose tissue, delayed spermatogenesis and incomplete lung development. Histological analysis reveals thick lung septa, small alveoli, diminished size and stratification of the adrenal cortex, and abnormally small anterior pituitary. Homozygous females are unable to deliver pups (dystocia) and do not lactate (agalactosis). Homozygous males are fertile. Sperm from homozygotes have increased binding to unfertilized eggs, bind ZP3 (zona pellucida glycoprotein 3) less and demonstrate poor zona pellucida penetration when compared to sperm from wildtype controls. Although able to undergo normal acrosomal exocytosis induced by calcium ionophore, homozygous sperm do not exhibit acrosome reaction to zona pellucida glycoproteins or anti-galactosyltransferase antibodies. Serum levels of thyroxine (T4) and T3 is reduced during the neonate period and then return to normal. Liver enzymes are elevated. This mutant mouse strain may be useful in studies of glycosidic molecular interactions and function, and polyglandular endocrine insufficiency.
This strain was transferred from the collection of the Consortium for Functional Glycomics.
B4galt1tm2Shur 006943Under Development for Production
B6.129S7-B4galt1tm2Shur /J
Strain Description These mice carry a mutant allele that has a point mutation in the first translation initiation codon in exon 1, which initiates translation of the long isoform of beta 1,4-galactosyltransferase. The second translation initiation codon in exon 1 is not affected. These mice express only the shorter isoform of beta 1,4-galactosyltransferase. No long isoform protein is detected in mammary tissue by Western blot analysis. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Total Beta 1,4-galactosyltransferase activity is reduced to 72% of wildtype levels in mammary gland epithelial cells while activity on mammary epithelial cell surfaces is diminished by over 60%. Sperm and testis exhibit near wildtype levels of enzyme activity and glycoprotein galactosylation. The short isoform is expressed ectopically in sperm. Although able to undergo normal acrosomal exocytosis induced by calcium ionophore, homozygous sperm do not exhibit acrosome reaction to zona pellucida glycoproteins or anti-galactosyltransferase antibodies. Homozygous females exhibit abnormal mammary gland morphology including excessive mammary epithelial duct branching. Approximately 20% of homozygous females do not support their young. Mutants have elevated levels of expression of metalloproteinases (Mmp14 and Mmp7). Laminin espression in basal lamina is abnormal. This mutant mouse strain may be useful in studies of glycosidic molecular interactions and function, and cell-to-extracellular matrix (ECM) interactions.
This strain was transferred from the collection of the Consortium for Functional Glycomics.
Bchetm1Loc 008077Under Development for Production
129S1/Sv-Bchetm1Loc /J
Strain Description Mice homozygous for this BChE mutant allele are viable and fertile with no reported spontaneous abnormalities. All tissues and plasma from homozygous mice are devoid of BChE activity. As BChE (butyrylcholinesterase) is a bioscavenger molecule protecting acetylcholinesterase (AChE) activity against nerve agents and organophosphates, homozygous BChE-deficiency leads to impaired protection from toxic compounds. These BChE mutant mice are a model for human butyrylcholinesterase deficiency and may be useful for studying metabolic effects of organophosphorus toxicants or nerve agents, neurotransmitter function, and anti-Alzheimer's drug therapies.
Of note, the donating investigator has multiple strains available that may be useful for testing toxic compounds, including the AChe-deficient (Stock No. 005987 ), G117H BChE transgenic (Stock No. 007577 ), and BChE-deficient (see Stock No. 008077 and Stock No. 008087 ) mice.
Bchetm1Loc 008087Under Development for Production
B6.129S1-Bchetm1Loc /J
Strain Description Mice homozygous for this BChE mutant allele are viable and fertile with no reported spontaneous abnormalities. All tissues and plasma from homozygous mice are devoid of BChE activity. As BChE (butyrylcholinesterase) is a bioscavenger molecule protecting acetylcholinesterase (AChE) activity against nerve agents and organophosphates, homozygous BChE-deficiency leads to impaired protection from toxic compounds. These BChE mutant mice are a model for human butyrylcholinesterase deficiency and may be useful for studying metabolic effects of organophosphorus toxicants or nerve agents, neurotransmitter function, and anti-Alzheimer's drug therapies.
Of note, the donating investigator has multiple strains available that may be useful for testing toxic compounds, including the AChe-deficient (Stock No. 005987 ), G117H BChE transgenic (Stock No. 007577 ), and BChE-deficient (see Stock No. 008077 and Stock No. 008087) mice.
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. As the BChE mutation was originally described on a 129S1/Sv genetic background (129S1-BChE mice), it should be noted that the phenotype of B6-BChE mice could vary from that originally described. We will modify the strain description if necessary as published results become available.
Car14tm1Sly 008218Under Development for Production
B6.129S1-Car14tm1Sly /J
Strain Description Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by RT-PCR or Western blot analysis of brain, heart, kidney, liver, and muscle tissue. Homozygotes exhibit reduced flash electroretinograms (rod/cone a-wave, b-wave, and cone b-wave) when compared to wildtype controls. The abnormal retinal light response of homozygotes is stable over time. This mutant mouse strain may be useful in studies of extracellular retinal pH and carbon dioxide regulation, photoreceptor response and retinal function.
Car3tm1Gkim 005358Under Development for Cryo
129S6/SvEvTac-Car3tm1Gkim /J
Strain Description Mice homozygous for the targeted allele are viable, fertile, normal in size and life span and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected. Histological examination of tissues discerns no anomalies. Similarly, gas chromatography-mass spectrometry analysis of the fatty-acid distribution in serum, muscle, liver, and fat reveal no differences between mutant and wildtype mice. When exposed to an atmosphere of 100% oxygen homozygous mice display similar mean survival times as wildtype (~ 70 hours). The contractile properties of soleus muscle derived from mutant mice exhibit some differences from wildtype mice. Mutant mice display shorter relaxation and half-relaxation times for single and tetanic twitches and a minor reduction tetanic force. Microarray analysis detects an increase (~30%) in carbonic anhydrase 13 expression.
Car4tm1Sly 008217Under Development for Production
B6.129S1-Car4tm1Sly /J
Strain Description Mice that are homozygous for this targeted mutation exhibit decreased sensitivity to an inhibitor of pH regulation (benzolamide) in the extracellular space in the hippocampus when compared to wildtype controls. No gene product (mRNA or protein) is detected by RT-PCR or Western blot analysis of brain, heart, kidney, liver, and muscle tissue. Exons 1b, 2, and 3, a portion of exon 4, which encode three active-site His residues, are disrupted and results in early termination in exon 4. Fewer than expected homozygotes are produced from heterozygote crosses (with even fewer female homozygotes produced). Surviving homozygotes from heterozygote crosses are fertile when crossed to wildtype mice, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous crosses produce small litters and pups do not survive. This mutant mouse strain may be useful in neuronal physiology related studies, especially those involving pH shifts that accompany neuronal activity.
Cav1tm1Mls 007083Under Development for Production
B6.Cg-Cav1tm1Mls /J
Strain Description Mice that are homozygous for the targeted mutation are viable, fertile and do not display any gross physical abnormalities. Mutant mice exhibit exercise intolerance when challenged and are slightly hyperphagic. No gene product (protein) is detected by Western blot analysis in adipose, lung and heart tissues or in cultured mouse embryonic fibroblasts (MEFs). A decrease in the level of co-expressed caveolin-2 protein is immunodetected. At age 4-5 months, mutant mice are often smaller than their wildtype littermates. By one year of age, mutant mice weigh 5 to 7 grams less than wildtype, and are resistant to diet-induced obesity. Progressive adipose pathology results in reduced white adipose tissue with abnormally small adipocytes and enlarged, hyperplastic brown adipose tissue. Homozygotes display lipid metabolism and uptake disruption with elevated serum triglycerides and free fatty acid levels, and reduced leptin levels. Isolated aortic tissue segments have a diminished vasoconstriction response to the alpha-1-adrenergic receptor agonist, phenylephrine, and an enhanced vasorelaxation response to acetylcholine. Histological examination of lung tissue from mutant mice shows thickened alveolar septa, hypercellularity, reduced alveolar spaces and increased density of basement membranes and reticulin fibers. Further immunohistochemical examination of lung tissue shows an increased number of endothelial cells. Mutant derived MEF cells proliferate two times faster and are denser at confluence as indicated by growth curves and cell cycle analysis. Electron microscopy analysis reveals a complete absence of caveolae (plasmalemmal vesicles) in endothelial cells. In vitro studies measuring uptake of fluorescently-labeled albumin and in vivo studies following uptake of gold-conjugated albumin demonstrate caveolar endocytosis impairment. This mutant mouse strain may be useful in studies of vesicular and cholesterol trafficking, signal transduction and tumorigenesis.
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. This is the case for the strain above. 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.
Ccr3tm1Cge 005440Under Development for Production
C.129S4-Ccr3tm1Cge /J
Strain Description Mice homozygous for this CCR3 (chemokine (C-C motif) receptor 3) targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RNA protection assay analysis of thymus, spleen and lung tissues. Mice homozygous for the mutation have impaired trafficking of eosinophils. A 7-fold decrease in the number of eosinophils in the small intestine and a 6-fold increase in the spleen is observed. Aerosol allergen challenge does not cause the expected infiltration of eosinophils to the lung tissue and airway lumens (50-70% reduction), although abundant eosinophils are found in the airway blood vessels. Concurrent increases in eosinophils in the spleen and intraepithelial mast cells in the spleen occur after allergen challenge. Homozygotes exhibit increased bronchoconstriction with allergen-induced airway hyperresponsiveness. There is no increase in eosinophils or eosinophil product major basic protein (MBP) in the skin after epicutaneous allergen treatment. Homozygous mice that have been epicutaneously sensitized do not develop increased airway responsiveness, or AHR, following inhalation challenge. These CCR3 mutant mice may be useful in studies of atopic dermatitis, allergic asthma, increased airway responsiveness/airway hyperresponsiveness (AHR).
Cd19tm1(cre)Cgn 007900Under Development for Production
C57BL/6-Gt(ROSA)26Sortm1(HBEGF)Awai /J
Strain Description Mice homozygous for this iDTR mutation are viable and fertile. These mice have the simian Diphtheria Toxin Receptor (DTR; from simian Hbegf ) inserted into the Gt(ROSA)26Sor (ROSA26) locus. Widespread expression of DTR is blocked by an upstream loxP -flanked STOP sequence. When bred to Cre recombinase-expressing mice, the STOP sequence is deleted in tissues where Cre is present, permitting DTR expression. Cells expressing DTR are rendered susceptible to ablation following Diphtheria toxin administration.
For example, when bred to a strain with a Cd19 null allele and expressing Cre recombinase during the B lymphocyte development (Stock No. 006785 ), this mutant mouse strain may be useful in studies of lymphocyte cell ablation.
Cd19tm1(cre)Cgn 008242Under Development for Production
C57BL/6-Gt(ROSA)26Sortm1(Ikbkb)Mass /J
Strain Description Mice homozygous for the R26StopFL ikk2ca conditional allele are viable and fertile, with a loxP -flanked STOP cassette preventing transcription of the downstream bicistronic sequences (a FLAG-tagged, constitutively active form of IKbkb (IKK2ca) and EGFP). When bred to mice that express Cre recombinase, the resulting offspring will have the STOP cassette deleted in the cre -expressing tissue(s); resulting in expression of the IKK2ca as well as EGFP fluorescence. Expression of IKK2ca leads to constitutively active NF-kappaB transcription factor activity. These R26StopFL ikk2ca mice allow inducible expression of an activated form of Ikbkb (IKK2 or IKK-beta) and subsequent activation of the NF-kappaB transcription factor pathways.
For example, when bred to a strain with a Cd19 null allele and expressing Cre recombinase during the B lymphocyte development (Stock No. 006785 ), this mutant mouse strain may be useful in studies of the NF-kappaB pathway.
Cd22tm1Lam 006940Under Development for Production
C57BL/6-Cd22tm1Lam /J
Strain Description Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No expression of the targeted gene's protein product is detected on the cell surface, as determined by flow cytometry analysis of splenocytes from homozygotes. Mutants exhibit a reduction in recirculating mature B cells in the bone marrow and fewer transitional B cells in the spleen. Splenic and peripheral B cells express lower levels of membrane bound IgM than wildtype. B cell activation is abnormal in mutant mice, with enhanced Ca2+ mobilization after stimulation. Lipopolysaccaharide (LPS) challenge results in an increased proliferative response. CD22 deficient B cells have a shorter than average lifespan when compared to wildtype B cells. T-cell independent immune responses are impaired. This mutant mouse strain may be useful in studies of glycosidic molecular interactions and function, B cell development and T cell independent immune response.
This strain was transferred from the collection of the Consortium for Functional Glycomics.
Cd74tm1Doi 008224Under Development for Production
NOD.129S2(B6)-Cd74tm1Doi /LwnJ
Strain Description Mice homozygous for the Cd74 targeted mutation are viable and fertile. Cd74 deficiency affects CD4 T cell development; therefore these mice have very few CD4+ T cells. Antigen presenting cells have reduced, though not abolished, ability to present MHC class II antigens, such as GAD . These mice are protected from diabetes. This stock is important for investigation of MHC class II molecule associated self-antigen selection and the importance of self-peptide in CD4 T cell selection and development.
Cdh23ahl 000668On Hold
C57L/J
Strain Description C57L/J mice are used widely in research as a general purpose strain. Mice have a high incidence of Hodgkin's-like reticulum cell neoplasm at 18 months of age and pituitary tumors in old multiparous females. C57L/J mice are highly susceptible to experimental allergic encephalomyelitis (EAE). In addition, C57L/J mice are highly susceptible to developing atherosclerotic aortic lesions (4500 to 8000 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat) (Paigen et al. 1990). On a lithogenic diet, C57L/J mice develop gallstones as a result of abnormal regulation of cholesterol synthesis (Xua et al., 2004). C57L/J mice carry no detectable endogenous ecotropic MuLV DNA sequences.
Cdh2tm1Glr 007611Under Development for Production
B6.129S6(SJL)-Cdh2tm1Glr /J
Strain Description These mice possess loxP sites on either side of exon 1 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 1 deleted in the cre -expressing tissue(s).
When bred to a strain with inducible Cre recombinase expression in cardiac cells (see Stock No. 005657 for example), this mutant mouse strain may be useful in studies of myocardium physiology.
Cx3cr1tm1Litt 008451Under Development for Production
B6.129P(Cg)-Ptprca Cx3cr1tm1Litt /LittJ
Strain Description Mice that are homozygous for the CX3CR1-GFP targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. RT-PCR analysis of lymphoid tissue from homozygotes detects mutant gene product (mRNA) and no wild type gene product (mRNA). Flow cytometric analysis of peripheral blood cells identified a subset of green fluorescent cells not observed in wild type mice. Enhanced Green Fluorescent Protein (EGFP), but not the endogenous gene, is expressed in monocytes, dendritic cells, NK cells, and brain microglia, mimicking endogenous gene expression. The same subset of peripheral blood cells isolated from heterozygote mice express detectable levels of EGFP. Immunohistochemical analysis of spleen and peripheral nerve tissue from homozygotes does not detect EGFP. These mice also express the CD45.1 (Ly5.1 or Ptprca ) allele, which is atypical for the C57BL/6 congenic background, and this marker may be used to track donor cell populations in transplantation studies with C57BL/6 (CD45.2, Ly5.2 or Ptprcb ) mice. These CX3CR1-GFP mice may be useful in studies of leukocyte migration and trafficking, as well as for transplantation studies.
Of note, CX3CR1-GFP mice are also available with the Ptprcb allele normally found in the C57BL/6 genetic background (see Stock No. 005582 ).
D11Mit168 008058Under Development for Production
NOD.L-(D11Mit314-D11Mit339 )(D11Mit364-D11Mit168 )/McdfJ
Strain Description This NOD congenic strain, commonly referred to as NOD.Lc11g or DR3g carries Chr. 11 alleles, D11Mit314 (51Mb) through D11Mit339 (63Mb) and D11Mit364 (72Mb) through D11Mit168 (113Mb) derived from C57L/J, which includes candidate gene Csf2 and Stat5a/Stat5b/Stat3 as well as Idd4.1 , Idd4.2 . Diabetes incidence in this strain is reported to be about 21% in females compared to 70% in female NOD control mice. (Davoodi-Semiromi et al, 2007).
This strain is useful to further study the role of Csf2 and Stat5a/Stat5b/Stat3 alleles in autoimmune disorders; to identify candidate diabetes resistant genes in the Idd4.1 and Idd4.2 regions and to positionally clone the Idd4 diabetes resistant loci.
D11Mit314 008058Under Development for Production
NOD.L-(D11Mit314-D11Mit339 )(D11Mit364-D11Mit168 )/McdfJ
Strain Description This NOD congenic strain, commonly referred to as NOD.Lc11g or DR3g carries Chr. 11 alleles, D11Mit314 (51Mb) through D11Mit339 (63Mb) and D11Mit364 (72Mb) through D11Mit168 (113Mb) derived from C57L/J, which includes candidate gene Csf2 and Stat5a/Stat5b/Stat3 as well as Idd4.1 , Idd4.2 . Diabetes incidence in this strain is reported to be about 21% in females compared to 70% in female NOD control mice. (Davoodi-Semiromi et al, 2007).
This strain is useful to further study the role of Csf2 and Stat5a/Stat5b/Stat3 alleles in autoimmune disorders; to identify candidate diabetes resistant genes in the Idd4.1 and Idd4.2 regions and to positionally clone the Idd4 diabetes resistant loci.
D11Mit339 008058Under Development for Production
NOD.L-(D11Mit314-D11Mit339 )(D11Mit364-D11Mit168 )/McdfJ
Strain Description This NOD congenic strain, commonly referred to as NOD.Lc11g or DR3g carries Chr. 11 alleles, D11Mit314 (51Mb) through D11Mit339 (63Mb) and D11Mit364 (72Mb) through D11Mit168 (113Mb) derived from C57L/J, which includes candidate gene Csf2 and Stat5a/Stat5b/Stat3 as well as Idd4.1 , Idd4.2 . Diabetes incidence in this strain is reported to be about 21% in females compared to 70% in female NOD control mice. (Davoodi-Semiromi et al, 2007).
This strain is useful to further study the role of Csf2 and Stat5a/Stat5b/Stat3 alleles in autoimmune disorders; to identify candidate diabetes resistant genes in the Idd4.1 and Idd4.2 regions and to positionally clone the Idd4 diabetes resistant loci.
D11Mit364 008058Under Development for Production
NOD.L-(D11Mit314-D11Mit339 )(D11Mit364-D11Mit168 )/McdfJ
Strain Description This NOD congenic strain, commonly referred to as NOD.Lc11g or DR3g carries Chr. 11 alleles, D11Mit314 (51Mb) through D11Mit339 (63Mb) and D11Mit364 (72Mb) through D11Mit168 (113Mb) derived from C57L/J, which includes candidate gene Csf2 and Stat5a/Stat5b/Stat3 as well as Idd4.1 , Idd4.2 . Diabetes incidence in this strain is reported to be about 21% in females compared to 70% in female NOD control mice. (Davoodi-Semiromi et al, 2007).
This strain is useful to further study the role of Csf2 and Stat5a/Stat5b/Stat3 alleles in autoimmune disorders; to identify candidate diabetes resistant genes in the Idd4.1 and Idd4.2 regions and to positionally clone the Idd4 diabetes resistant loci.
D13Mit314 006061Under Development for Cryo
B6.D2-(D13Mit314 -D13Mit35 )/1LusJ
Strain Description This C57BL/6J congenic carries the distal portion of chromosome 13 from DBA/2J. The Mit or SNP (rs) markers in the strain name define the congenic interval. Marker-assisted breeding was used to construct a set of overlapping congenic strains called genome-tagged mice (GTM) that span the entire mouse genome. Each member of the panel carries an average of a 23 cM segment (range 8 to 58 cM) from DBA/2J introgressed on to a C57BL/6J background. The segments represent the distal (D), middle (M), and proximal (P) portions of all or most of a given chromosome. (Iakoubova OA, et. al., 2001) GTM are a valuable resource for mapping and confirmation of loci contributing to complex traits.
The Jackson Laboratory is working with Dr. Lusis' group to import and make available additional strains in the panel.
D13Mit35 006061Under Development for Cryo
B6.D2-(D13Mit314 -D13Mit35 )/1LusJ
Strain Description This C57BL/6J congenic carries the distal portion of chromosome 13 from DBA/2J. The Mit or SNP (rs) markers in the strain name define the congenic interval. Marker-assisted breeding was used to construct a set of overlapping congenic strains called genome-tagged mice (GTM) that span the entire mouse genome. Each member of the panel carries an average of a 23 cM segment (range 8 to 58 cM) from DBA/2J introgressed on to a C57BL/6J background. The segments represent the distal (D), middle (M), and proximal (P) portions of all or most of a given chromosome. (Iakoubova OA, et. al., 2001) GTM are a valuable resource for mapping and confirmation of loci contributing to complex traits.
The Jackson Laboratory is working with Dr. Lusis' group to import and make available additional strains in the panel.
D2Mit405 005154Under Development for Cryo
B6.D2-(D2Mit405 -D2Mit457 )/LusJ
Strain Description This C57BL/6J congenic carries the distal portion of chromosome 2 from DBA/2J. The Mit or SNP (rs) markers in the strain name define the congenic interval.
Marker-assisted breeding was used to construct a set of overlapping congenic strains called genome-tagged mice (GTM) that span the entire mouse genome. Each member of the panel carries an average of a 23 cM segment (range 8 to 58 cM) from DBA/2J introgressed on to a C57BL/6J background. The segments represent the distal (D), middle (M), and proximal (P) portions of all or most of a given chromosome. (Iakoubova OA, et. al., 2001) GTM are a valuable resource for mapping and confirmation of loci contributing to complex traits.
The Jackson Laboratory is working with Dr. Lusis' group to import and make available additional strains in the panel.
D2Mit405 006059Under Development for Production
B6.CAST-(D2Mit405-D2Mit74 )/LusJ
Strain Description This C57BL/6J congenic carries the proximal portion of chromosome 2 from CAST/Ei. The Mit or SNP (rs) markers in the strain name define the congenic interval. Marker-assisted breeding was used to construct a set of overlapping congenic strains called genome-tagged mice (GTM) that span the entire mouse genome. Each member of the panel carries an average of a 23 cM segment (range 8 to 58 cM) from CAST/Ei introgressed on to a C57BL/6J background. The segments represent the distal (D), middle (M), and proximal (P) portions of all or most of a given chromosome. (Iakoubova OA, et. al., 2001) GTM are a valuable resource for mapping and confirmation of loci contributing to complex traits.
The Jackson Laboratory is working with Dr. Lusis' group to import and make available additional strains in the panel.
D2Mit457 005154Under Development for Cryo
B6.D2-(D2Mit405 -D2Mit457 )/LusJ
Strain Description This C57BL/6J congenic carries the distal portion of chromosome 2 from DBA/2J. The Mit or SNP (rs) markers in the strain name define the congenic interval.
Marker-assisted breeding was used to construct a set of overlapping congenic strains called genome-tagged mice (GTM) that span the entire mouse genome. Each member of the panel carries an average of a 23 cM segment (range 8 to 58 cM) from DBA/2J introgressed on to a C57BL/6J background. The segments represent the distal (D), middle (M), and proximal (P) portions of all or most of a given chromosome. (Iakoubova OA, et. al., 2001) GTM are a valuable resource for mapping and confirmation of loci contributing to complex traits.
The Jackson Laboratory is working with Dr. Lusis' group to import and make available additional strains in the panel.
D2Mit74 006059Under Development for Production
B6.CAST-(D2Mit405-D2Mit74 )/LusJ
Strain Description This C57BL/6J congenic carries the proximal portion of chromosome 2 from CAST/Ei. The Mit or SNP (rs) markers in the strain name define the congenic interval. Marker-assisted breeding was used to construct a set of overlapping congenic strains called genome-tagged mice (GTM) that span the entire mouse genome. Each member of the panel carries an average of a 23 cM segment (range 8 to 58 cM) from CAST/Ei introgressed on to a C57BL/6J background. The segments represent the distal (D), middle (M), and proximal (P) portions of all or most of a given chromosome. (Iakoubova OA, et. al., 2001) GTM are a valuable resource for mapping and confirmation of loci contributing to complex traits.
The Jackson Laboratory is working with Dr. Lusis' group to import and make available additional strains in the panel.
D8Mit318 005174Under Development for Cryo
B6.D2-(D8Mit318 -D8Mit56 )/LusJ
Strain Description This C57BL/6J congenic carries the distal portion of chromosome 8 from DBA/2J. The Mit or SNP (rs) markers in the strain name define the congenic interval. Marker-assisted breeding was used to construct a set of overlapping congenic strains called genome-tagged mice (GTM) that span the entire mouse genome. Each member of the panel carries an average of a 23 cM segment (range 8 to 58 cM) from DBA/2J introgressed on to a C57BL/6J background. The segments represent the distal (D), middle (M), and proximal (P) portions of all or most of a given chromosome. (Iakoubova OA, et. al., 2001) GTM are a valuable resource for mapping and confirmation of loci contributing to complex traits.
The Jackson Laboratory is working with Dr. Lusis' group to import and make available additional strains in the panel.
D8Mit56 005174Under Development for Cryo
B6.D2-(D8Mit318 -D8Mit56 )/LusJ
Strain Description This C57BL/6J congenic carries the distal portion of chromosome 8 from DBA/2J. The Mit or SNP (rs) markers in the strain name define the congenic interval. Marker-assisted breeding was used to construct a set of overlapping congenic strains called genome-tagged mice (GTM) that span the entire mouse genome. Each member of the panel carries an average of a 23 cM segment (range 8 to 58 cM) from DBA/2J introgressed on to a C57BL/6J background. The segments represent the distal (D), middle (M), and proximal (P) portions of all or most of a given chromosome. (Iakoubova OA, et. al., 2001) GTM are a valuable resource for mapping and confirmation of loci contributing to complex traits.
The Jackson Laboratory is working with Dr. Lusis' group to import and make available additional strains in the panel.
D9Mit115 005175Under Development for Cryo
B6.D2-(D9Mit329 -D9Mit115 )/LusJ
Strain Description This C57BL/6J congenic carries the middle portion of chromosome 9 from DBA/2J. The Mit or SNP (rs) markers in the strain name define the congenic interval. Marker-assisted breeding was used to construct a set of overlapping congenic strains called genome-tagged mice (GTM) that span the entire mouse genome. Each member of the panel carries an average of a 23 cM segment (range 8 to 58 cM) from DBA/2J introgressed on to a C57BL/6J background. The segments represent the distal (D), middle (M), and proximal (P) portions of all or most of a given chromosome. (Iakoubova OA, et. al., 2001) GTM are a valuable resource for mapping and confirmation of loci contributing to complex traits.
The Jackson Laboratory is working with Dr. Lusis' group to import and make available additional strains in the panel.
D9Mit329 005175Under Development for Cryo
B6.D2-(D9Mit329 -D9Mit115 )/LusJ
Strain Description This C57BL/6J congenic carries the middle portion of chromosome 9 from DBA/2J. The Mit or SNP (rs) markers in the strain name define the congenic interval. Marker-assisted breeding was used to construct a set of overlapping congenic strains called genome-tagged mice (GTM) that span the entire mouse genome. Each member of the panel carries an average of a 23 cM segment (range 8 to 58 cM) from DBA/2J introgressed on to a C57BL/6J background. The segments represent the distal (D), middle (M), and proximal (P) portions of all or most of a given chromosome. (Iakoubova OA, et. al., 2001) GTM are a valuable resource for mapping and confirmation of loci contributing to complex traits.
The Jackson Laboratory is working with Dr. Lusis' group to import and make available additional strains in the panel.
Ddr2slie 008172Under Development for Production
BKS(HRS)-Ddr2slie /JngJ
Strain Description Mice homozygous for this mutation appear normal at birth. By weaning, they exhibit a reduced body mass, gain weight slower and display minor craniofacial abnormalities such as protruding eyes and a shortened snout. Bone mineral content, but not density is reduced in homozygotes. Plasma glucose levels are significantly increased while blood urea nitrogen levels are decreased in homozygotes. By six weeks, it can be seen that homozygous females lack a corpora lutea. By four months, homozygous males exhibit atrophy of spermatogonia, Sertoli and Leydig cells. This mutant mouse strain has characteristics similar to human Levi type dwarfism and may be useful in studies related to dwarfism and infertility.
Dicer1tm1Bdh 006366Under Development for Production
B6.Cg-Dicer1tm1Bdh /J
Strain Description These mice contain loxP sites on either side of exon 23. Homozygous mice are viable and fertile with no gross phenotypic or behavioral abnormalities. Expression of the targeted allele is indistinguishable from wildtype despite the frt -flanked neomycin cassette. Cre-mediated recombination (resulting in deletion of exon 23) in the germline leads to developmental arrest at embryonic day 7.5 (E7.5). Tissue specific deletion has been shown to result in loss of microRNA (miRNA) processing. Mutant mice can be used to generate cell/tissue-specific deletions of the endogenous gene for applications in embryonic development, translation, protein processing and miRNA/siRNA regulation of gene expression.For example, when crossed to a strain expressing Cre recombinase in mesenchyme (see Stock No. 005584 ), this mutant mouse strain may be useful in studies of limb morphogenesis.
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.
Dldtm1Ptl 008333Under Development for Production
B6;129P2-Dldtm1Ptl /J
Strain Description Mice heterozygous for the Dld (dihydrolipoamide dehydrogenase or E3 component) targeted mutation are viable and fertile. Heterozygous mice exhibit approximately half of wild-type enzymatic activity levels for E3 and all affected mitochondrial multienzyme complexes. Heterozygotes (on a C57BL/6;129P2 genetic background) exhibit increased vulnerability to treatments with MPTP (dopaminergic neurotoxin used to induce Parkinson's disease-like lesions), malonate (inhibitor of cellular respiration used to mimic Huntington's disease features), and 3-NP (mitochondrial toxin used to mimic Huntington's disease features). Homozygous mice exhibit normal development and metabolism during the preimplantation period, explained by the persistence of E3 enzyme from the oocyte. Homozygotes exhibit developmental delays shortly after implantation (7.5 to 8.5 days postcoitum (dpc)) and cease development within the subsequent 2 days. These Dld mutant mice may be useful to study early murine embryonic metabolism, including glucose and mitochondrial metabolism during the early postimplantation period. As altered energy metabolism and reductions in alpha-ketoacid dehydrogenase complexes have also been associated with many neurodegenerative disorders, these mice may also be useful for studying Parkinson's disease, Huntington's disease, and/or Alzheimer's disease. Because the metabolic disturbances associated with E3 deficiency (Dld deficiency) cause a variant of Maple Syrup Urine Disease (MSUD) in which there is an accompanying lactic acidosis due to concomitant deficiency of pyruvate dehydrogenase complex, these mice may be useful in such studies or in conjunction with iMSUD mice (Stock No. 006999 ).
EdaTa-6J 001809On Hold
B6-Aw-J .Cg-EdaTa-6J +/+ ArTfm /J
Strain Description Testicular feminization (ArTfm ) is a dominant spontaneous mutation on the X chromosome. Hemizygous male mice are outwardly female in appearance except that the vagina does not open until 3 months of age if at all. Male reproductive development is abnormal leading to very small testes, and the absense of vas deferens, the epididymis, and male accessory glands. Spermatogonia and Sertoli cells are present in the testes, but spermatogenesis does not proceed past meiotic prophase. Leydig cells, which normally produce androgen in males, fail to develop normally. This strain is also segregating for the tabby 6J mutation (EdaTa-6J ) that affects both the coat color and hair pattern growth. The tabby mutation is maintained in repulsion with the testicular feminization mutation and is used as a coat color marker to assist in identifying resulting genotypes obtained from matings.
EdaTa 000314On Hold
B6CBACa Aw-J /A-EdaTa /J-XO
Strain Description
Edardl-J 000255On Hold
GL/Le Edardl-J +/+ Ostm1gl /J
Strain Description Mice homozygous for the grey-lethal spontaneous mutation (Ostm1gl ) are characterized by osteopetrosis. Homozygous mutant mice are anemic, have a reduced white cell count, early thymic involution, and deficient calcium regulation. Homozygotes lack the power of secondary bone resorption. Consequently, the bones cannot grow normally, they do not form normal marrow cavities, and the teeth do not erupt.
Efna2tm1Jgf 005992Under Development for Production
STOCK Efna2tm1Jgf Efna5tm1Ddmo /J
Strain Description Mice homozygous for both targeted mutations are viable, fertile, and normal in size. 10-20% of females homozygous at both loci neglect their litters. Double homozygous mice have no endogenous protein expression in inferior colliculus (IC) or superior colliculus (SC), and thus lack the concentration gradient created by the endogenous proteins across the midbrain in wildtype mice. Temporal and nasal retinal axon termination is severely altered: multiple ectopic aborizations in the SC indicate abnormalities in both anteroposterior and dorsoventral topography. Following surgical ablation of portions of the midbrain (including IC and SC), cross-modal innervation by retinal neurons is greater in double homozygous mutants compared to wildtype. Mice heterozygous at both loci have greater reproductive performance compared to homozygotes. Further, double heterozygotes have temporal (but not nasal) retinal axon aborization in the SC with diminished frequency and severity. These ephrin A2/ephrin A5 double mutant mice may be useful in studies of retinocollicular mapping, axon topography, neuron projection, and modality-specific compartmentalization of visual, auditory, and somatosensory thalamic relay pathways.
Efna5tm1Ddmo 005992Under Development for Production
STOCK Efna2tm1Jgf Efna5tm1Ddmo /J
Strain Description Mice homozygous for both targeted mutations are viable, fertile, and normal in size. 10-20% of females homozygous at both loci neglect their litters. Double homozygous mice have no endogenous protein expression in inferior colliculus (IC) or superior colliculus (SC), and thus lack the concentration gradient created by the endogenous proteins across the midbrain in wildtype mice. Temporal and nasal retinal axon termination is severely altered: multiple ectopic aborizations in the SC indicate abnormalities in both anteroposterior and dorsoventral topography. Following surgical ablation of portions of the midbrain (including IC and SC), cross-modal innervation by retinal neurons is greater in double homozygous mutants compared to wildtype. Mice heterozygous at both loci have greater reproductive performance compared to homozygotes. Further, double heterozygotes have temporal (but not nasal) retinal axon aborization in the SC with diminished frequency and severity. These ephrin A2/ephrin A5 double mutant mice may be useful in studies of retinocollicular mapping, axon topography, neuron projection, and modality-specific compartmentalization of visual, auditory, and somatosensory thalamic relay pathways.
Epas1tm1Mcs 008407Under Development for Production
STOCK Epas1tm1Mcs /J
Strain Description These mice possess loxP sites on either side of exon 2 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon deleted in the cre -expressing tissue(s).
When bred to a strain with inducible Cre recombinase expression in cardiac cells (see Stock No. 005657 for example), this mutant mouse strain may be useful in studies of erythropoiesis.
Epb4.1l3tm1Jkis 007681Under Development for Production
STOCK Epb4.1l3tm1Jkis /J
Strain Description Mice homozygous for this 4.1B/Dal-1 targeted allele are viable, fertile, and age normally with no spontaneous tumor formation. Lung, brain, breast, and prostate tissues from homozygotes show no protein expression from the mutant locus. Although 4.1B-deficient females do not form tumors of the mammary gland, a significant increase in mammary epithelial cell proliferation during pregnancy is observed. When these 4.1B-deficient mice are bred with TRAMP transgenic mice (see Sock No. 003135 ), the resulting double mutant offspring exhibit increased susceptibility for developing aggressive prostate carcinomas and enhanced tumor malignancy associated with reduced apoptosis. Because 4.1B expression is frequently downregulated in human clinical prostate cancer (and a spectrum of other tumor types), these 4.1B mutant mice may be useful in studying the role of 4.1B as a negative regulator of cancer progression to metastatic disease.
Eraftm1.1Mjwe 007858Under Development for Production
B6.129S6(Cg)-Eraftm1.1Mjwe /J
Strain Description Mice homozygous for this targeted allele (AHSP-/- or ERAF-/- ) are fertile with normal lifespans up to at least 18 months of age. No RNA or protein from the targeted gene is detected in hematopoietic tissues from homozygotes. AHSP-/- mice exhibit abnormal erythrocyte morphology with intracellular inclusion bodies that stain positively for denatured hemoglobin (Heinz bodies). Homozygous mice also have reduced lifespan of circulating red blood cells, increased apoptosis of erythroid precursors, and increased production of reactive oxygen species (ROS) with consequent damage to hemoglobin A and other cellular components. As the a -hemoglobin stabilizing protein specifically binds the cytotoxic free a -Hb subunit of hemoglobin A, these AHSP-mutant mice may be useful in studying erythroid development/erythropoiesis, thalassemia, Heinz body hemolytic anemia, and other hemoglobinopathies.
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. As AHSP-mutant mice were originally described on a mixed C57BL/6 and 129 genetic background, 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.
Foxp3sf 006775On Hold
NOD.Cg-Foxp3sf /DoiJ
Strain Description Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. By 3 weeks of age, Foxp3 -deficient NOD mice suffer massive lymphoproliferation and inflammatory infiltration in lungs, liver, skin, pancreas, kidneys, stomach, colon, fat and muscles and die by three weeks of age. At 14 days of age, NOD.Foxp3 -deficient mice developed exocrine pancreatitis and occasional peri-insulitis; however invasive insulitis and diabetes were not observed.
In a NOD.Foxp3 -deficient, BDC2.5 TCR transgenic model, mice experienced markedly decreased lymphoproliferation, yet 100% were diabetic by 20 days of age.
This congenic NOD scurfy model is useful to study the role of Foxp3 -dependent regulatory T cells on diabetes development.
Fut1tm1Sdo 006939Under Development for Production
B6.129-Fut1tm1Sdo /J
Strain Description Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Alpha(1,2)fucosylated glycans are not detected in the epididymis of homozygotes. Fucosylated glycolipids (fucosyl GA1) are not detected in the pancreatic acinar glands of homozygotes. Homozygotes exhibit delayed maturation of nerve fibers in the glomerular layer of the olfactory bulb due to absence of cell surface carbohydrate, blood group H carbohydrate, expression in primary sensory neurons. The Donating Investigator reports that the beta-galatosidase is expressed. This mutant mouse strain may be useful in studies of glycosidic molecular interactions and function, and olfactory nerve pathway development.
This strain was transferred from the collection of the Consortium for Functional Glycomics.
Gabrb3tm1Geh 002711Under Development for Production
B6;129-Gabrb3tm1Geh /J
Strain Description The gamma-Aminobutyric acid type A receptors mediate the majority of rapid inhibitory synaptic transmission in the CNS. The beta3 subunit is an essential component of these receptors in many brain regions, especially during development, and is implicated in several pathophysiologic processes. The majority of mice homozygous for the Gabrb3tm1Geh mutation (or beta3-/-) die at birth with ~60% displaying cleft palate and the remaining ~35% die for unidentified reasons. Homozygous females that survive are fertile but do not care for their pups. Survivors have frequent myoclonus and occasional epileptic seizures, are hypersensitive to external stimuli and handling, have a lack of coordination and display altered responses to certain anesthesias. In addition, the observed behavioral deficits (especially regarding social behaviors) indicate that mutant mice may be a useful model of autism spectrum disorders.Of note, several strains bearing gamma-aminobutyric acid (GABA-A) receptor mutations are available from this donating investigator (Dr. Gregg Homanics, University of Pittsburgh), including Gabra1 (Stock No. 004318 ), Gabra4 (Stock No. 006874 ), Gabra6 (Stock No. 002710 ), Gabrb3 (Stock No. 002711 ), Gabrd (Stock No. 003725 ), and Gabrg2 (Stock No. 003137 ).
Gabrb3tm2.1Geh 008310Under Development for Production
B6;129-Gabrb3tm2.1Geh /J
Strain Description These mice possess loxP sites on either side of exon 3 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 3 deleted in the cre -expressing tissue(s). When bred to a strain expressing Cre recombinase in the neuronal cells (see Stock No. 003966
for example), this mutant mouse strain may be useful in studies of neurodevelopmental diseases.
When bred to a strain expressing Cre recombinase in the hippocampal CA1 pyramidal cell layer (see Stock No. 005359
for example), this mutant mouse strain may be useful in studies of neurodevelopmental diseases.
Of note, several strains bearing gamma-aminobutyric acid (GABA-A) receptor mutations are available from this donating investigator (Dr. Gregg Homanics, University of Pittsburgh), including Gabra1 (Stock No. 004318 ), Gabra4 (Stock No. 006874 ), Gabra6 (Stock No. 002710 ), Gabrb3 (Stock No. 002711 and Stock No. 008310 ), Gabrd (Stock No. 003725 ), and Gabrg2 (Stock No. 003137 ).
Gata4tm1.1Sad 008194Under Development for Production
STOCK Gata4tm1.1Sad /J
Strain Description Mice homozygous for this Gata4loxP conditional allele are viable and fertile, with loxP sites flanking exons 3-5 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region (coding for both zinc finger DNA-binding domains and the nuclear localization signal essential for GATA4 function) deleted in the cre -expressing tissue(s). These GATA binding protein 4 conditional mice may be useful in generating conditional mutations for studying GATA4 function during organogenesis (such as cardiogenesis) or in adult mice.
Gata6tm2.1Sad 008196Under Development for Production
STOCK Gata6tm2.1Sad /J
Strain Description Mice homozygous for this Gata6loxp conditional allele are viable and fertile, with loxP sites flanking exon 2 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region (coding for the majority of the GATA6 protein) deleted in the cre -expressing tissue(s). These Gata6loxp mice may be useful in generating conditional GATA binding protein 6 mutations for studying GATA6 function in organogenesis or in adult mice.
For example, when bred to a strain expressing Cre recombinase in the villi and crypt cells of the intestine (see Stock No. 004586 for example), or when bred to a strain expressing Cre recombinase in the embryo (see Stock No. 003724 , 003314 for example), this mutant mouse strain may be useful in studies of the transcription factor Gata6 .
Gata6tm2.2Sad 008196Under Development for Production
STOCK Gata6tm2.1Sad /J
Strain Description Mice homozygous for this Gata6loxp conditional allele are viable and fertile, with loxP sites flanking exon 2 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region (coding for the majority of the GATA6 protein) deleted in the cre -expressing tissue(s). These Gata6loxp mice may be useful in generating conditional GATA binding protein 6 mutations for studying GATA6 function in organogenesis or in adult mice.
For example, when bred to a strain expressing Cre recombinase in the villi and crypt cells of the intestine (see Stock No. 004586 for example), or when bred to a strain expressing Cre recombinase in the embryo (see Stock No. 003724 , 003314 for example), this mutant mouse strain may be useful in studies of the transcription factor Gata6 .
Gli1tm3(cre/ESR1)Alj 007913Under Development for Production
STOCK Gli1tm3(cre/ESR1)Alj /J
Strain Description Mice homozygous for this Gli1-CreERT2 targeted allele are viable and fertile (although homozygous males are reported to have breeding problems). Under control of the endogenous upstream promoter/enhancer elements, tamoxifen-inducible cre activity is observed in cells that have received positive Hedgehog/Sonic Hedgehog signaling. The Cre-ERT2 fusion protein consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17b -estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen and, with lesser sensitivity, ICI 182780. Restricted to the cytoplasm, Cre-ERT2 can only gain access to the nuclear compartment after exposure to tamoxifen. To counteract the mixed estrogen agonist effects of tamoxifen injections, which can result in late fetal abortions in pregnant mice, progesterone may be coadministered. When these Gli1-CreERT2 mice are bred with mice containing a loxP -flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the flanked sequences in Gli1 expressing cells; making them useful for studying axis patterning, proliferation, and cell fate specification of Hedgehog responding cells at different stages of embryogenesis.
Gpi1b 005730Under Development for Cryo
129S6.CB(B6)-Del(1)1Brk Gpi1b /Gpi1c /BrkMdfJ
Strain Description Homozygous mice develop microcytic anemia, sparse hair, enlarged spleens and a slight cardiomegaly. Males are infertile. Homozygous mice on the C57BL/6J background develop hydrocephalus and less than 5% survive beyond 6 days. On the 129 background, 95% of mice survive to adulthood.
Grin3btm1Yaha 007808Under Development for Production
B6.129P2-Grin3btm1Yaha /J
Strain Description Mice homozygous for this NR3B (Grin3b ) mutant allele are viable and fertile, with no RNA from the targeted allele expressed in adult spinal cord. Homozygotes show a moderate but significant impairment in motor learning or coordination, decreased body weight with age, and decreased activity in their home cages. In addition, homozygous mice exhibit highly increased social interactions with their familiar cage mates in their home cage, with moderately increased anxiety-like behavior and decreased social interaction in novel environments. These NR3B (Grin3b ) mutant mice may be useful in neurobiological studies; specifically studies involving NMDA receptor and NR3B function in cranial and spinal somatic motor neurons.
Gt(ROSA)26Sortm1(HBEGF)Awai 007900Under Development for Production
C57BL/6-Gt(ROSA)26Sortm1(HBEGF)Awai /J
Strain Description Mice homozygous for this iDTR mutation are viable and fertile. These mice have the simian Diphtheria Toxin Receptor (DTR; from simian Hbegf ) inserted into the Gt(ROSA)26Sor (ROSA26) locus. Widespread expression of DTR is blocked by an upstream loxP -flanked STOP sequence. When bred to Cre recombinase-expressing mice, the STOP sequence is deleted in tissues where Cre is present, permitting DTR expression. Cells expressing DTR are rendered susceptible to ablation following Diphtheria toxin administration.
For example, when bred to a strain with a Cd19 null allele and expressing Cre recombinase during the B lymphocyte development (Stock No. 006785 ), this mutant mouse strain may be useful in studies of lymphocyte cell ablation.
Gt(ROSA)26Sortm1(Ikbkb)Mass 008242Under Development for Production
C57BL/6-Gt(ROSA)26Sortm1(Ikbkb)Mass /J
Strain Description Mice homozygous for the R26StopFL ikk2ca conditional allele are viable and fertile, with a loxP -flanked STOP cassette preventing transcription of the downstream bicistronic sequences (a FLAG-tagged, constitutively active form of IKbkb (IKK2ca) and EGFP). When bred to mice that express Cre recombinase, the resulting offspring will have the STOP cassette deleted in the cre -expressing tissue(s); resulting in expression of the IKK2ca as well as EGFP fluorescence. Expression of IKK2ca leads to constitutively active NF-kappaB transcription factor activity. These R26StopFL ikk2ca mice allow inducible expression of an activated form of Ikbkb (IKK2 or IKK-beta) and subsequent activation of the NF-kappaB transcription factor pathways.
For example, when bred to a strain with a Cd19 null allele and expressing Cre recombinase during the B lymphocyte development (Stock No. 006785 ), this mutant mouse strain may be useful in studies of the NF-kappaB pathway.
Gt(ROSA)26Sortm1(Notch1)Dam 008159Under Development for Production
STOCK Gt(ROSA)26Sortm1(Notch1)Dam /J
Strain Description These mice contain a sequence encoding an intracellular portion of the mouse Notch1 gene (amino acids 1749-2293), but lacking the c-terminal PEST domain, and Green Fluorescent Protein, GFP, inserted into the GT(ROSA)26Sor locus. Expression of the Notch1 fragment and GFP is blocked by a loxP-flanked STOP fragment placed between the coding sequence and the GT(ROSA)26Sor promoter. The GFP expression is localized to the nucleus by an IRES sequence. The truncated cytoplasmic fragment encoded by the Notch1 sequence causes constitutive signaling activity. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants for studying the effects of Notch pathway activation. Homozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities.
For example, when crossed to a strain expressing a tamoxifen inducible Cre recombinase in all cells that express Shh (see Stock No. 005623 ), this mutant mouse strain may be useful in studies of Notch signalling.
Gucy2dtm1Mom 006703Under Development for Cryo
B6;129P2-Gucy2dtm1Mom /MomJ
Strain Description
Gusbtm3Sly 005644Under Development for Production
B6.129X-Gusbtm3Sly /J
Strain Description Homozygous mice are viable but infertile. Fertility can be restored with enzyme replacement therapy. Less than 1% residual enzyme activity is observed. Homozygous mice are indistinguishable from wild type mice at birth, but show distinct growth retardation, shortened extremities, and facial dysmorphism observable at three months with a moderate increase in severity with age. Long bones of the lower extremities are shortened, broad, and sclerotic. Compared to wild type, this model has increased urinary glycosaminoglycan and secondary elevation of other lysosomal storage enzymes. Further, homozygous mice show abundant lysosomal storage in liver, kidney, leptomeningeal cells, cornea, and retinal pigment epithelium. The phenotype exhibited by this mutant mouse strain is less severe than that observed in a similarly constructed mutant (Stock No. 005643 ) which bears a E536A point mutation. This strain represents a model of human GUS deficiency characterized by the most prevalent human mutation, L176F, and is associated with mild Mucopolysaccharidosis type VII (MPS VII or Sly Syndrome).
H2 001626Under Development for Cryo
NOD.NON-H2nb1 /LtJ
Strain Description This congenic strain carries the diabetes-resistant MHC from the NON/LtJ strain (Stock No. 002423) and is used as a comparison to the NOD/LtJ (Stock No. 001976). These mice exhibit some but not all of the immune dysfunctions of NOD/LtJ mice. These mice are useful for dissecting the role of MHC versus non-MHC genes in producing aberrant immunophenotypes.
H2d 000359On Hold
B6.C-H2d /bByJ
Strain Description
H2g7 001627Under Development for Cryo
NON.NOD-H2g7 /LtJ
Strain Description This congenic strain carries the diabetogenic MHC from NOD/LtJ mice and is used as a comparison strain for NOD/LtJ (Stock No. 001976) and NON/LtJ (Stock No. 002423). These mice exhibit some but not all of the immune dysfunctions of NOD/LtJ mice. These mice are useful for dissecting the role of MHC versus non-MHC genes in producing aberrant immunophenotypes.
Hlxtm1Rph 008313Under Development for Production
B6.129P2-Hlxtm1Rph /J
Strain Description Homozygous null mice have an embryonic lethal phenotype. Homozygous mice on the C57BL/6 and B6;129 mixed background fail to develop past embryonic days 15.5 due to impaired fetal hematopoiesis (anemia, hypoplastic and abnormal development of the liver, hypoplastic gut). Homozygous mice on the FVB/N background survive through embryonic day 18.5 and dead homozygote newborn pups are observed. Late gestation homozygous embryos on the FVB/N background are smaller than wildtype littermates, pale, hydropic (subcutaneous fluid ballooning skin), and have impaired neural crest cell and enteric neuron migration from the stomach to intestine. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Naive CD4 T cells from heterozygotes exhibit increased responsiveness to IL-4, resulting in differentiation of more Th2 cells. This mutant mouse strain may be useful in studies of liver and gastrointestinal development and T helper 2 cell differentiation.
Hlxtm1Rph 008315Under Development for Production
FVB.129P2(Cg)-Hlxtm1Rph /J
Strain Description Homozygous null mice have an embryonic lethal phenotype. Homozygous mice on the C57BL/6 and B6;129 mixed background fail to develop past embryonic days 15.5 due to impaired fetal hematopoiesis (anemia, hypoplastic and abnormal development of the liver, hypoplastic gut). Homozygous mice on the FVB/N background survive through embryonic day 18.5 and dead homozygote newborn pups are observed. Late gestation homozygous embryos on the FVB/N background are smaller than wildtype littermates, pale, hydropic (subcutaneous fluid ballooning skin), and have impaired neural crest cell and enteric neuron migration from the stomach to intestine. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Naive CD4 T cells from heterozygotes exhibit increased responsiveness to IL-4, resulting in differentiation of more Th2 cells. This mutant mouse strain may be useful in studies of liver and gastrointestinal development and T helper 2 cell differentiation.
Hmox1tm1Poss 008311Under Development for Production
FVB.129S2(B6)-Hmox1tm1Poss /J
Strain Description Mice that are homozygous for this targeted mutation are slightly smaller in size than wildtype littermates and exhibit poor grooming and hypoactivity. As early as 20 weeks of age, homozygotes develop anemia with diminished serum iron and increased serum ferritin. Histological analysis reveals iron accumulation in kidney and liver. Elevated oxidized proteins and lipid peroxidation develop in the liver and kidney. Homozygotes develop progressive chronic inflammatory
disease, including enlarged spleen and lymph nodes, inflammatory infiltrates, glomerulonephritis, fibrosis. Homozygous male mice have smaller testis than wildtype controls. Homozygotes occur at a lower than expected frequency, or are not produced, from heterozygous crosses and have decreased postnatal survival. An almost undetectable abnormal gene product (mRNA) is detected by Northern blot analysis of total splenic RNA. This mutant mouse strain may be useful in studies of hemochromatosis, inflammation and iron metabolism.
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. This is the case for the strain above. 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.
Htttm2Detl 004595On Hold
B6.129P2-Htttm2Detl /J
Strain Description Mice homozygous for the targeted allele are viable and fertile. At 15-40 weeks of age mice carrying this allele on a segregating C57BL/6 and 129P2 background exhibit an abnormal gait, clasping behavior and diminished exploratory activity. Infrequent tonic-clonic like seizures may also be observed. Mice with a higher percentage of C57BL/6 in their genetic background develop behavioral and neurological phenotypes at a much later age (70-100 weeks). (Heng MY et al., 2007) Mutant mice may be noticeably smaller than wild-type littermates. Increased glial fibrillary acidic protein immunoreactivity is present in the striatum and ubiquititin- and huntingtin-positive neuronal intranuclear inclusions (NIIs) are detected throughout the dorsal striatum, nucleus accumbens and to a lesser extent other regions of the brain. Onset of symptoms occurs earlier for homozygotes than for heterozygotes.This mutant mouse strain represents a model that may be useful in studies related to Huntington's disease.
Hydinhy3 002703On Hold
B6CBACa Aw-J /A -Hydinhy3 /J
Strain Description Mice homozygous for the hydrocephalus 3 spontaneous mutation (Hydinhy3 ) are usually identifiable at 3 to 5 days. Those with frank hydrocephalus die by 4 or 5 weeks of age. The lateral ventricles and the third ventricle are enlarged, the aqueduct of Sylvius and the fourth ventricle are only slightly affected, and there is some dilatation of the ventral subarachnoid cistern. The hydrocephalus seems to be due to a defect in the subarachnoid space under the calvarium caused by an abnormal postnatal differentiation of the arachnoid mater and pia mater which prevents their separation. Penetrance is incomplete.
Idd3C57BL/6 007934Under Development for Production
NOD.B6(PL)-Idd3C57BL/6 /MrkTacJ
Strain Description This NOD congenic strain, commonly referred to as NOD.B6-Idd3 , commonly referred to as NOD.B6-Idd3R450, is carrying Chr 3 alleles, rs3022959 through rs3140619, derived from strain C57BL/6 including the insulin dependent diabetes susceptibility 3 loci (Idd3 ). This NOD.B6 congenic strain is diabetes resistant, with approximately 10% of the females becoming diabetic by 250 days of age. Activated and non-activated thymocytes and splenocytes of this T1D protected stock produce more Il2 mRNA than T1D susceptible strains (Stock No's. 007930 , 007931 , and 007932 ). This congenic strain, one of a set of 5 strains (Stock No's. 007930 , 007931 , 007932 , and 007933 ), has been useful to positionally clone Idd3 , to study the biological effects of variation of genes within the Idd3 region, specifically the Il2 gene and continues to be valued for studying long-range chromosome remodeling.
Ins2Akita 006580Under Development for Production
B6.Cg-Ins2Akita Ldlrtm1Her /J
Strain Description Mice homozygous for the Akita spontaneous mutation die postnatally, typically by 12 weeks of age. Independently, heterozygous Akita mutant mice are a model of insulin dependent diabetes mellitus (IDDM) with severe hyperglycemia (see the datasheet for Stock No. 003548 for additional information). LDLR-null homozygotes have elevated serum cholesterol levels (200-400 mg/dl) which can escalate to very high levels (> 2000 mg/dl) when the mice are fed a high fat diet. LDLR-deficient mice also are predisposed to develop atherosclerosis. These double mutant mice may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, hypercholesterolemia, and diabetes-related macrovascular complications.
Itga5tm1Hyn 002274On Hold
B6.129S-Itga5tm1Hyn /J
Strain Description Mice homozygous for the Itga5tm1Hyn targeted mutation die during embryonic development. Homozygous mutant embryos exhibit defects in the vasculature of the yolk sac and the embyro as well as severe defects in posterior and extraembryonic mesoderm. Implantation and initiation of gastrulation and neurulation is normal. There is normal development of notochord, somite and considerable development of brain, optic and otic anlagen and branchial arches.
L1camtm1Sor 003518Under Development for Cryo
129/Sv-L1camtm1Sor /J
Strain Description The L1 gene is localized to the X chromosome. As a result, hemizygous males are affected and the mutation has to be propagated through females. Male mice hemizygous for the L1camtm1Sor targeted mutation have defects in the guidance of axons of the corticospinal tract. A substantial proportion of axons do not take their normal crossed course to the dorsal column at the pyramidal decussation. There is also a varying, but reduced number of corticospinal axons in the dorsal columns of the spinal cord.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.
L1camtm1Sor 003120Under Development for Cryo
B6;129S7-L1camtm1Sor /J
Strain Description The L1 gene is localized to the X chromosome. As a result, hemizygous males are affected and the mutation has to be propagated through females. Male mice hemizygous for the L1camtm1Sor targeted mutation have defects in the guidance of axons of the corticospinal tract. A substantial proportion of axons do not take their normal crossed course to the dorsal column at the pyramidal decussation. There is also a varying, but reduced number of corticospinal axons in the dorsal columns of the spinal cord.
Ldlrtm1Her 006952Under Development for Production
B6.Cg-Akt2tm1.1Mbb Ldlrtm1Her /J
Strain Description Independently, homozygous Akt2 mutant mice develop insulin resistance and diabetes, while LDLR homozygotes are predisposed to atherosclerosis. Double mutant mice that are heterozygous for the Akt2 allele and homozygous for the LDLR mutation are viable and fertile. These double mutant mice may be useful in studies of diabetes, metabolism, hyperglycemia, and atherosclerosis.
Ldlrtm1Her 006580Under Development for Production
B6.Cg-Ins2Akita Ldlrtm1Her /J
Strain Description Mice homozygous for the Akita spontaneous mutation die postnatally, typically by 12 weeks of age. Independently, heterozygous Akita mutant mice are a model of insulin dependent diabetes mellitus (IDDM) with severe hyperglycemia (see the datasheet for Stock No. 003548 for additional information). LDLR-null homozygotes have elevated serum cholesterol levels (200-400 mg/dl) which can escalate to very high levels (> 2000 mg/dl) when the mice are fed a high fat diet. LDLR-deficient mice also are predisposed to develop atherosclerosis. These double mutant mice may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, hypercholesterolemia, and diabetes-related macrovascular complications.
Ltb4r1tm1Adl 008102Under Development for Production
B6.129S4-Ltb4r1tm1Adl /J
Strain Description Mice homozygous for this BLTR (BLT1)-deficient allele are viable and fertile. Northern blot analysis of neutrophils, macrophages, lymph nodes, lungs, and
spleens isolated from homozygous mice show absence of the normal transcript and presence of the expected larger transcript (due to the insertion of the neomycin resistance cassette in exon 2 of the targeted gene), albeit at lower levels than the wild type transcript. Homozygous disruption of this allele confers impaired leukocyte function (chemotaxis, recruitment, firm adhesion). For example, homozygotes exhibit substantially diminished recruitment of eosinophils in a model of peritonitis, effector T cells in a model of allergic pulmonary inflammation, and neutrophils in a model of rheumatoid arthritis. As the G protein-coupled receptor BLTR/BLT1 is expressed on myeloid leukocytes (including neutrophils, macrophages, eosinophils, T cell lymphomas, and effector T cells (TH1 CD4+ cells, TH2 CD4+ cells, and effector memory CD8+ cells) during CD4+ migration/recruitment from the lymphoid compartment into peripheral tissues), these BLTR/BLT1 mutant mice may be useful for studying leukocyte function in inflammation, as well as the role of the LTB4-BLT1 pathway linking early immune system activation and multiple classes of acquired immune effector cells.
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.
Mecp2tm1Bird 006847Under Development for Production
B6;129P2-Mecp2tm1Bird /J
Strain Description These mice possess two functional loxP sites flanking exons 3-4 of the targeted gene on the X chromosome. Homozygous females and hemizygous males are viable and fertile. Northern blot analysis showed the expected mature transcript from the Mecp2lox locus. Also detected was an unspliced beta-globin transcript that was introduced into the locus as part of the targeting vector. When these mutant mice are bred to mice that express cre recombinase, resulting offspring will have exons 3-4 deleted in the cre -expressing tissue(s). Mice with this X-linked floxed mutation may be useful in neurological and developmental studies of Rett syndrome. For example, when crossed to a strain expressing Cre recombinase in nervous tissue (see Stock No. 003771 ), this mutant mouse strain develops a neurological phenotype that mimics Rett syndrome.
Mgat5tm1Jwd 006335Under Development for Production
B6.129-Mgat5tm1Jwd /J
Strain Description No gene product (protein) is detected by Western blot analysis and enzyme activity is undetectable. Beta-galactosidase activity mimics endogenous gene expression patterns. Homozygotes exhibit abnormal increased leukocyte infiltration in kidney tissue, which is indicative of kidney autoimmune glomerulonephritis. Induced experimental autoimmune encephalomyelitis (EAE) and induced delayed-type hypersensitivity (DTH) responses are increased in homozygotes. Cultured splenocytes isolated from homozygotes produce 2 fold more IFN-gamma and 2 fold less IL4. Mutant mice exhibit delayed tumor progression when bred with oncomice (for example, when crossed to a polyomavirus middle T antigen expressing transgenic strain). Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator reports that homozygous females are not fertile. This mutant mouse strain may be useful in studies of glycosidic molecular interactions and function, autoimmunity and antitumor immunity.
This strain was transferred from the collection of the Consortium for Functional Glycomics.
Mgl1tm1Hed 006944Under Development for Production
B6.129-Mgl1tm1Hed /J
Strain Description Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by Northern blot or RT-PCR analysis. Immunohistochemical reactivity is not detected in inflamed skin. Although mutant mice exhibit slightly increased red blood cell counts, mean corpuscular hemoglobin, hematocrit and mean corpuscular volume when compared to wildtype controls, these levels are within the normal range for mice.
Homozygotes have diminished antigen-induced granulation tissue formation but show normal antigen-independent granulation tissue formation. This mutant mouse strain may be useful in studies of glycosidic molecular interactions and function, antigen-specific and antigen-independent cellular immune response and hematopoiesis.
Mirn150tm1Rsky 007750Under Development for Production
B6;C-Mirn150tm1Rsky /J
Strain Description Mice homozygous for this targeted allele (miR150-/- ) are viable and fertile with normal development of T cells, follicular B cells, and MZ B cells. No miR-150 is expressed in spleen, mesenteric lymph node, and thymus of homozygotes. Homozygous mice exhibit B cell expansion (CD19+ B220loCD5+ CD43+ CD23- ; B1a subset) in spleen and peritoneal cavity (with reciprocal reduction in B2 cells) and enhanced humoral immune response (increased serum immunoglobulins of various classes both at steady-state and following T cell-dependent antigen exposure). Homozygous miR-150 deficiency also leads to enhanced induction of the miR-150 target protein c-Myb in activated B and T cells, but no reported change in expression of the miR-150 target genes Foxp1 or ZFP91 in resting or activated B cells. These miR150-/- mice may be useful in mircoRNA biology, specifically to study the role of miR-150 and its target genes (including c-Myb) in lymphocyte development and function.
Mirn155tm1.1Rsky 007745Under Development for Production
B6.Cg-Mirn155tm1.1Rsky /J
Strain Description Mice homozygous for this loss-of-function/reporter allele (bic/mir-155-/-) are viable and fertile. The lacZ reporter allows the detection of bic promoter transcriptional activity using fluorescence activated cell sorting (FACS). In homozygotes, miR-155 expression is undetectable in activated splenic B cells. In heterozygotes, approximately 60% of germinal center (GC) B cells express the lacZ reporter whereas the vast majority of the non-GC B cells do not. Homozygous mice exhibit a reduced fraction of GC B cells in the gut-associated lymphoid tissue (GALT; including Peyer's patches (PPs) and mesenteric lymph nodes (mLNs)). In addition, bic/miR-155-/- B cells exhibit deficient tumor necrosis factor (TNF) and lymphotoxin-a (LT-a ) cytokine production. Homozygous mice show impaired T cell-dependent antibody responses, and their T cells show a TH2 cytokine bias (an increased percentage of interleukin-4 (IL-4) producing cells and a decreased percentage of interferon-g (IFN-g ) producing cells), accompanied by a higher fraction of cells producing IL-10. These bic/mir-155 mutant mice may be useful in mircoRNA biology, specifically to study the role of miR-155 and its target genes (including cytokines, chemokines, and transcription factors) in homeostasis and immune system function.
Mlphln 000668On Hold
C57L/J
Strain Description C57L/J mice are used widely in research as a general purpose strain. Mice have a high incidence of Hodgkin's-like reticulum cell neoplasm at 18 months of age and pituitary tumors in old multiparous females. C57L/J mice are highly susceptible to experimental allergic encephalomyelitis (EAE). In addition, C57L/J mice are highly susceptible to developing atherosclerotic aortic lesions (4500 to 8000 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat) (Paigen et al. 1990). On a lithogenic diet, C57L/J mice develop gallstones as a result of abnormal regulation of cholesterol synthesis (Xua et al., 2004). C57L/J mice carry no detectable endogenous ecotropic MuLV DNA sequences.
Mmp9tm1Tvu 007084Under Development for Production
B6.FVB(Cg)-Mmp9tm1Tvu /J
Strain Description Mice that are homozygous null for the Mmp9 gene are viable and fertile. No Mmp9 activity is detected in spleen cell lysates. Long bones (tibia, femur) are 10% shorter in homozygous null mice. Histological examination of 3-week-old mice reveals a dramatically l
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