Search Criteria: Research Area is "Neurobiology Research: Neural Tube Defects"

Additional Register Interest Strains

JAX® Mice Strains

Stock
Number
Strain Name
 
Strain Description
Standard Supply
006084 B6.129P2(Cg)-Foxg1tm1(cre)Skm/J
Repository- Live
This strain expresses Cre recombinase from the endogenous Foxg1 locus. Forkhead box G1 is required for telencephalon development and is expressed specifically in the telencephalon and discrete head structures. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in tissue-specific deletion of the target. Recombination occurs in the telencephalon, anterior optic vesicle (developing lens and retina), otic vesicle, facial and head ectoderm, olfactory epithelium, mid-hindbrain junction and pharyngeal pouches. Mice that are homozygous for the targeted mutation die perinatally. Heterozygous mutant mice are viable, fertile, normal in size. On the C57BL/6 background, forebrain volume in heterozygotes is substantially reduced especially in the cerebral cortex (40.7%), striatum (29.7%), and hippocampus (18.6%). In the adult, the thalamus is reduced in volume by 21.6%. This mutant mouse strain represents a model that ma .....
For more information please see the full phenotype on the strain data sheet
009107 B6.Cg-Tg(Wnt1-cre)11Rth Tg(Wnt1-GAL4)11Rth/J
Repository- Live
This strain is exhibiting white belly spotting. We are currently in the process of breeding away from this phenotype, but we are continuing to distribute this strain regardless of this spontaneous mutation. In 2011, Stock No. 009107 at The Jackson Laboratory Repository was confirmed to harbor the expected Wnt1-Cre transgene, as well as the originally co-injected Wnt1-GAL4 transgene. The strain phenotype description below has been updated accordingly.

When homozygous for both co-injected transgenes, Wnt-1/GAL4/cre-11 transgenic mice are viable and fertile. Of note for Wnt-1/GAL4/cre-11 transgenic mice on the original mixed genetic background, the donating investigator (Dr. Epstein) reported that homozygous mice may be lethal as some offspring from transgenic parents die around two months of age. Both Cre recombinase and the GAL4 transcriptional activator are expressed under the direction of wingless-related MMTV integration site 1 (Wnt1) promoter/regul .....
For more information please see the full phenotype on the strain data sheet

005549 B6;129-Pax3tm1(cre)Joe/J
Repository- Live
This strain expresses Cre recombinase from the endogenous Pax3 locus. Expression of the targeted gene product (mRNA and protein) mimics endogenous gene expression as detected by in situ hybridization and immunohistochemistry of homozygous embryos aged E12.5. No endogenous Pax3 gene product (protein) is detected in homozygotes and approximately one half of the endogenous gene product (protein) is detected in heterozygotes by Western blot analysis. Cre recombinase expression is detected in the dorsal neural tube and somites of E9 to 11.5 embryos and in the cardiac neural crest cells and colonic epithelia of E11.5 embryos. Recombination occurs in neural crest and somite derivatives of later gestation embryos. Homozygous mice have an embryonic lethal phenotype, failing to develop past embryonic day 18.5. At age E13.5 homozygous embryos display severe cardiac and neural tube defects (exencephaly), absent limb musculature and reduced or absent dorsal root ganglia. Heterozygous .....
For more information please see the full phenotype on the strain data sheet
004293 B6;129-Shhtm2Amc/J
Repository- Live
Mice that are homozygous for the Shhtm2Amc targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This conditional mutant contains two loxP sites flanking exon 2 of the targeted allele. Cre-mediated recombination excises exon 2 and some surrounding intronic sequence, generating a null allele. When the conditional mutant is crossed with a ubiquitously-expressing Cre recombinase carrier to remove Shh activity in the early embryo, the resulting phenotype resembles the Shh null mutation. These conditional mutant mice may be mated to strains expressing Cre recombinase to study the effects of temporal and tissue-specific ablation of the targeted allele. This mutant mouse strain represents a model that may be useful in studies of developmental defects resulting from disruption of Shh-dependent pathways.

When bred to a strain expressing Cre recombinase under the control of a tet .....
For more information please see the full phenotype on the strain data sheet

025250 B6.Cg-Csktm1Sor Tg(Csk*)2Weis/WeisJ
Under Development - Now Accepting Orders
Mice hemizygous for the BAC CskAS transgene are viable and fertile. These mice do not express the endogenous c-src tyrosine kinase (CSK) protein. These mice do express mutant CSK, from the BAC transgene, which contains a point mutation at position 266 resulting in a threonine to glycine mutation. This mutation creates a larger ATP-binding pocket in the expressed protein, allowing for specific and rapid inhibition by an analog of the kinase inhibitor PP1, 3-iodo-benzyl-PP1 (3-IB-PP1). CSK is a cytosolic tyrosine-protein kinase that plays a role in the regulation of cell growth, differentiation, migration and immune response. CSK phosphorylates tyrosine residues located in the C-terminal tails of Src-family kinases (SFKs), which in turn suppress signaling by surface receptors including T-cell receptor (TCR) and B-cell receptor (BCR). CskAS mice have 2.5-fold as much expression of CSK as wild-type mice and display normal T cell development. Inhibitio .....
For more information please see the full phenotype on the strain data sheet
024377 B6.Cg-Tg(TCF/Lef1-lacZ)34Efu/KatmJ
Under Development - Now Accepting Orders
The TOPGAL transgene has three TCF/LEF consensus binding sites and the minimal c-fos promoter controlling expression of β-galactosidase. TOPGAL activity (lacZ expression) is induced by β-catenin and correlates with canonical Wnt signaling. For example, lacZ expression is observed where β-catenin/Lef1 complexes are active, including the hair placodes and germs, as well as the developing mouse vestibular system (during anterior and posterior semicircular canal formation). Hemizygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The phenotype of B6.TOPGAL homozygous mice has not been characterized to date (February 2014).

The phenotype of hemizygous TOPGAL mice on the CD-1 genetic background is described for Stock No. 004623. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are freque .....
For more information please see the full phenotype on the strain data sheet

022135 STOCK Gbx2tm1.1(cre/ERT2)Jyhl/J
Under Development - Now Accepting Orders
The Gbx2cre/ER allele expresses a CreERT2-internal ribosome entry site (IRES)-enhanced green fluorescent protein (EGFP) cassette from the Gbx2 promoter/enhancer elements. Gbx2 is induced, and EGFP immunofluorescence is observed, in thalamic neuronal precursor cells in the diencephalon. Cre-ERT2 fusion gene activity is inducible; observed in the same cells only following tamoxifen administration. When Gbx2cre/ER mice are bred with mice containing loxP-flanked sequence, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequences in the Gbx2-expressing cells of the offspring. Heterozygous mice are viable and fertile. Homozygotes lack a cerebellum and thalamocortical projections, and die at birth.

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 (17 .....
For more information please see the full phenotype on the strain data sheet

023405 STOCK Tfap2atm1.1Hsv/J
Under Development - Now Accepting Orders
The AP-2alphaki knock-in/knockout allele has an IRES-lacZ cassette inserted into exon 7 of the transcription factor AP-2α gene; both abolishing endogenous gene function and placing lacZ expression under direction of the Tfap2a promoter/enhancer regions. Wildtype mice have AP-2alpha expression in the neural tube, and in cranial and cardiac neural crest cells in the developing embryo, as well as in the progress zone of the limb bud, the developing kidney, the eye, and surface ectoderm. Most homozygotes exhibit prenatal or postnatal lethality due to neural tube, craniofacial, body wall, and cardiac malfomation, while the majority of heterozygotes are viable and fertile. In these mice, β-gal labels the ectoderm, and cranial and cardiac neural crest populations during the E8.5-10.5. Homozygous mice exhibit failure of neural tube closure by E9.5, and outflow tract abnormalities from E14.5-15.5.
023406 STOCK Tfap2atm2Will/J
Under Development - Now Accepting Orders
These floxed-AP-2alpha mutant mice possess loxP sites flanking exons 5-6 of the transcription factor AP-2α gene. AP-2alpha is expressed in the neural tube, and in cranial and cardiac neural crest cells in the developing embryo, as well as in the progress zone of the limb bud, the developing kidney, the eye, and surface ectoderm. Mice that are homozygous for this allele are viable and fertile. When bred to mice that express tissue-specific Cre recombinase, resulting offspring will have exons 5-6 deleted in the cre-expressing tissues.

For example, when bred to B6.Cg-Tg(Wnt1-cre)11Rth Tg(Wnt1-GAL4)11Rth/J mice (Stock No. 009107) expressing Cre recombinase in the developing neural tube, offspring are perinatal lethal due neural tube closure defects and cleft secondary palate. Some mutant mice can survive into adulthood and exhibit retarded craniofacial growth, abnormal middle ear development, and de .....
For more information please see the full phenotype on the strain data sheet

004337 129(Cg)-Foxg1tm1(cre)Skm/J
Cryopreserved - Ready for recovery
This strain expresses Cre recombinase from the endogenous Foxg1 locus. Forkhead box G1 is required for telencephalon development and is expressed specifically in the telencephalon and discrete head structures. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in tissue-specific deletion of the target. Recombination occurs in the telencephalon, anterior optic vesicle (developing lens and retina), otic vesicle, facial and head ectoderm, olfactory epithelium, mid-hindbrain junction and pharyngeal pouches. Mice that are homozygous for the targeted mutation die perinatally. Heterozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain represents a model that may be useful in studies of telencephalic development.
009091 129-Skitm1Cco/J
Cryopreserved - Ready for recovery
Mice homozygous for the targeted mutation die before or shortly after birth due to developmental defects. More than 80% of homozygotes on the 129 background exhibit exencephaly (severe neural tube closure defects) between embryonic day 15.5 (E15.5) and embryonic day 18.5 (E18.5). None exhibit facial clefting. The Donating Investigator reports that homozygotes display flattened or shorter snouts, iris malformation and polydactyly. The penetrance of the phenotype is highly background dependent. Heterozygotes are viable and fertile with timely cranial neural tube closure and, the Donating Investigator reports, no facial clefting. This mutant strain may be useful in studies of facial cleft formation, 1p36 deletion syndrome, oncogene function, apoptosis, and neural tube and skeletal muscle defects.
005291 129-Tulp3tm1Jng/Pjn
Cryopreserved - Ready for recovery
003518 129/Sv-L1camtm1Sor/J
Cryopreserved - Ready for recovery
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.

000212 129P4.Cg-Axin1Fu/J
Cryopreserved - Ready for recovery
The fused mutation is dominant and generally more severe in homozygotes, but has highly varying penetrance in both the heterozygote and homozygote, to the extent that some homozygotes do not have an abnormal phenotype. Phenotypic traits of mice carrying the Axin1Fu allele include shortened, bifurcated, or absent tails, kinked tails with fused vertebrae, other asymmetrical fusions of vertebrae, axial duplications, and ribs fused at the proximal ends. Imperforate anus, anemia at birth, waltzing movement, deafness, and missing or abnormal kidneys have also been reported. Both heterozygotes and homozygotes are generally fertile although female carriers transmit with a lower penetrance than males do. (Reed, 1936; Dunn and Gluecksohn-Waelsch, 1954; Theiler and Gluecksohn-Waelsch, 1956.)
003201 129S-Csktm1Sor/J
Cryopreserved - Ready for recovery
Mice homozygous for disruption of the csk gene die in utero at 9 - 10 days of gestation, exhibiting defects in neurulation. Mutant embryos are anatomically indistinguishable from normal or heterozygous littermates at E8.5, but are identifiable at E9.5 by their smaller size, failure to 'turn' (reverse orientation of germ layers) and failure to close their cephalic neural folds. The allantois of these mutant embryos is also abnormal and does not connect with the chorion, preventing formation of the umbilical cord and placenta. The kinase Csk plays a role in negative regulation of the Src family tyrosine kinases by phosphorylating a key carboxy-terminal tyrosine residue. Expression of csk in normal embryos is detectable at low levels beginning at E8.5, and is at its highest level of expression at E9.5.
003383 129S-Nogtm1Amc/J
Cryopreserved - Ready for recovery
Homozygous mice are born but die shortly after birth, exhibiting multiple defects, including an open neural tube, skeletal abnormalities, shortened body axis, and a small vestigial tail. Analysis of early gene expression has shown that the loss of Nog expression in the floorplate, notochord, and roofplate results in a progressive failure of ventral development in the CNS and somites. Nog is also expressed in condensing cartilage in the limb and in the sclerotome of somites so its loss results in defects in cartilage patterning and skeletal morphogenesis. Heterozygous embryos show lacZ reporter expression in pattern consistent with the endogenous gene.
009085 129S/Sv-Rettm1Cos/J
Cryopreserved - Ready for recovery
The Ret- allele (also called ret-k-, ret-k minus, or c-ret-) disrupts the region of the ret proto-oncogene (Ret; also called ret-k or c-ret) locus harboring the invariant lysine codon required for Ret kinase activity. Homozygous mice die around 16-24 hours after birth, exhibiting abnormalities in kidney/urinary (renal agenesis/hypodysplasia) and peripheral nervous system development (including sympathetic, parasympathetic, and enteric ganglia), as well as abnormal enteric neural crest cell migration. Because homozygous mice lack enteric ganglia from the hindgut, these mice are also a model of Hirschsprung's Disease.
016157 129S1.B6-Shroom3m1Nisw/J
Cryopreserved - Ready for recovery
Mice heterozygous for the ENU-induced mutation, Shroom3C5745T, are viable and fertile, although homozygotes die shortly before birth. These mice possess a C to T mutation in the codon for amino acid residue 1663 results in an arginine to cysteine change in the shroom family member 3 (Shroom3) gene. These mice exhibit complete exencephaly (hind-mid-forebrain), cleft face, and body wall defects. These mutant mice may be useful in studying embryonic development.
009092 A.129P-Skitm1Cco/J
Cryopreserved - Ready for recovery
Mice homozygous for the targeted mutation die before or shortly after birth due to developmental defects. Homozygotes on the A/J background exhibit exencephaly (severe neural tube closure defects), with a higher embryonic lethality than homozygotes on the C57BL/6 or 129 backgrounds. None exhibit facial clefting. The Donating Investigator reports that homozygotes display flattened or shorter snouts, iris malformation and polydactyly. The penetrance of the phenotype is highly background dependent. Heterozygotes are viable and fertile with timely cranial neural tube closure, and a low incidence of facial clefting. The Donating Investigator reports some heterozygotes on the A/J background exhibit lateral facial clefting. This mutant strain may be useful in studies of facial cleft formation, 1p36 deletion syndrome, oncogene function, apoptosis, and neural tube and skeletal muscle defects.
005136 A/WySnJ-ctl/GrsrJ
Cryopreserved - Ready for recovery
Mice homozygous for the ctl mutation are easily recognizable at birth by their curly or bent tails.
002991 B6.129-Ascl1tm1And/J
Cryopreserved - Ready for recovery
Mice homozygous for the Ascl1tm1And targeted mutation die within 24 hours after birth. There are no gross external defects; However, mutant mice do have extensive loss of sympathetic ganglia and olefactory epithelium.
002957 B6.129-Dll1tm1Gos/J
Cryopreserved - Ready for recovery
Mouse embyros homozygous for the Dll1tm1Gos targeted mutation establish a primary metameric pattern in the mesoderm. Cytodifferentiation appears normal, but the segments have no cranio-caudal polarity, and no epithelial somites form. Caudal sclerotome halves do not condense, and the pattern of spinal ganglia and nerves is perturbed, indicating loss of segment polarity. Myoblasts span segment borders, demonstrating that these borders are not maintained.
003537 B6.129-Kif3atm1Gsn/J
Cryopreserved - Ready for recovery
Ciliary formation appears to be crucial in developing left-right asymmetry in early mouse embryonic development. One of the necessary cilia components is the Kif3a gene product. Homozygous Kif3a knockout mice die at 10 days postcoitum, exhibit randomized establishment of left-right asymmetry and display numerous structural abnormalities. Cardiac looping is randomized, often retarded. Growth is severely retarded with caudal truncation. A neural tube closure defect is also apparent. Scanning electron microscopy indicates the absence of embryonic cilia. A small percentage of heterozygotes exhibit morphological abnormalities.
005709 B6.129-Skitm1Cco/J
Cryopreserved - Ready for recovery
This mutant was created on a mixed (129 x C57BL/6J) background. Greater than 80% of mice on this mixed background had severe neural tube closure defects (such as exencephaly) while less than 16% exhibited facial clefting. The penetrance of these phenotypes has segregated with further backcross to C57BL/6J. The congenic mutant described here was backcrossed 12-14 times to wildtype C57BL/6J. Mice homozygous for the targeted mutation die before or shortly after birth due to developmental defects. Null mice are distinguishable from wildtype and heterozygous littermates at embryonic day 8.5 (E8.5) with delayed, but complete, cranial neural tube closure (incomplete at the normal E9.5). Ninety percent of null mice alive at E18.5 exhibit facial clefting. Other highly penetrant phenotypes include flattened snout, depressed nasal bridge, excessive orbital separation, elongated subventricular zones, vestigial polydactyly, and malformations of the olfactory bulb, iris, and ventral septum. Heterozy .....
For more information please see the full phenotype on the strain data sheet
005290 B6.129-Tulp3tm1Jng/Pjn
Cryopreserved - Ready for recovery
018054 B6.129P2(Cg)-Pitx2tm1.1Dmm/J
Cryopreserved - Ready for recovery
In this mutant strain an IRES Tau-lacZ cassette replaces exon 4 of the paired-like homeodomain transcription factor 2 (Pitx2) gene, abolishing expression of all three PITX2 isoforms. PITX2 is a transcription factor expressed in the developing mammillary and retromammillary regions of the hypothalamus. PITX2 is involved in memory processing by regulating neural axonal migration. Heterozygous Pitx2tlz/+ mice are viable and fertile, while homozygous Pitx2tlz/tlz mice exhibit embryonic lethality. Pitx2tlz/+ embryos show lacZ staining in the eye, pituitary, teeth, heart, craniofacial regions, and neural tube. The brains of heterozygous embryos show lacZ staining the hypothalamus and midbrain. Pitx2tlz/tlz embryos exhibit defects of the heart, abdominal viscera, and distal turning. They have improperly bundled and disorganized axonal fibers in the primary mammillary tract which are still .....
For more information please see the full phenotype on the strain data sheet
002053 B6.129P2-Apobtm1Unc/J
Cryopreserved - Ready for recovery
The Apobtm1Unc targeted mutation produces a truncated form of the apolipoprotein B protein (APOB70)and no apoB100 that is similar to human familial hypobetalipoproteinemia condition. Expression of apoB48 is not altered. Homozygous mice show greatly reduced levels of plasma APOB, beta-lipoproteins, and total cholesterol. They also have reduced plasma triglyceride concentrations, fasting chylomicronemia, and reduced high density lipoprotein (HDL) cholesterol. Homozygotes also have a high incidence of exencephaly and hydrocephaly. Heterozygous mice show a slight increase over wildtype in the incidence of hydrocephaly.
003821 B6.129S1-Twist1Pde/J
Cryopreserved - Ready for recovery
015829 B6.129S2-Pak4tm1Amin/J
Cryopreserved - Ready for recovery
In this strain, a neo cassette replaces exon 1 of the p21 protein (Cdc42/Rac)-activated kinase 4 (Pak4) gene, abolishing gene expression. Heterozygotes are viable, fertile, normal in size, and do not display any gross physical abnormalities. Homozygotes die by E11.5 due to fetal heart defects. Pak4 is a member of the group B family of PAK serine/threonine kinases and is expressed early in development in a variety of tissues. It is involved in the formation of filopodia in response to Cdc42, promoting neuronal growth. Improper folding of the caudal neural tubes of homozygous embryos results in the formation of two neural lumens. They also exhibit abnormalities in the development, migration and differentiation of neurons. Specifically, axonal outgrowth was impaired, and neurons failed to migrate to their proper locations. These mice may be useful for studying the role of Pak4 in embryonic and neuronal development.
003754 B6.129S4-Shroom3Gt(ROSA53)Sor/J
Cryopreserved - Ready for recovery
Mice that are homozygous for this mutation survive to term or die very shortly after birth. The gene trap insertion appears to have occurred between the translational start sites of the long and short forms in the 5' portion of the endogenous gene. No gene product (protein or mRNA) is detected in homozygous embryos. Mutant embryos can be distinguished by E9.25 as the lateral edges of the cranial neural folds exhibit a wavy appearance and fail to converge at the dorsal midline. As the embryo develops, the neural folds continue to enlarge and develop away from the dorsal midline, presenting a mushroom-like appearance. By day E14.5, failed neural tube closure results in exencephaly, acrania, and facial clefting. Some mutants exhibit defects in ventral closure resulting in herniation of the intestine and liver. Not all aspects of the phenotype are fully penetrant. Hemizygous mice express a B-galactosidase under the control of the endogenous promoter, with expression variously observed .....
For more information please see the full phenotype on the strain data sheet
004069 B6.129S6-Crebbptm1Dli/J
Cryopreserved - Ready for recovery
Mice that are homozygous null for the Crebbp gene are embryonic lethal, dying at about embryonic day 10.5 exhibiting open neural tube defects. Heterozygous mice though viable and fertile, are subject to early growth retardation, craniofacial abnormalities and often fail to thrive. Heterozygous mice are also subject to age-dependent splenomegaly and irregular hematopoiesis. By three months of age, the abundance of all hematopoietic cell types is significantly diminished. Older mice (10-21 months) are more prone to develop hematologic malignancies than wildtype mice.
002222 B6.129S7-Twist1tm1Bhr/J
Cryopreserved - Ready for recovery
Homozygotic embryos for the Twist1tm1Bhr targeted mutation die at 11.5. The most prominent phenotype is a failure of cranial neural tube closure. At embryonic day 8.5 the cranial neural folds are elevated but not fused. At embryonic day 9.5 exencephaly is evident (the cranial neuroepithelium is everted and exposed). There is also abnormal somite morphology and abnormal limb bud development.
004202 B6.C3 Pde6brd1 Hps4le/+ +-Lmx1adr-8J/J
Cryopreserved - Ready for recovery
000026 B6.C3-Gli3Xt-J/J
Cryopreserved - Ready for recovery
Mice heterozygous for the extra toes-J spontaneous mutation (Gli3Xt-J) have varying numbers of extra digits on preaxial side of feet. Homozygous mutant mice die in utero with multiple abnormalities. Excessively large pharyngeal arches and an open neural tube are evident at E9. Homologous to Grieg's cephalopoly-syndactyly, a rare multi-system syndrome in humans.
000311 B6.Cg-Pax3Sp N/J
Cryopreserved - Ready for recovery
Mice homozygous for the splotch spontaneous mutation (Pax3Sp) die at E13 due to neural tube defects. Malformations of homozygous mutant embryos include rachischisis in the lumbosacral region and frequently in the region of the hindbrain. Heterozygous splotch mice show white spotting on the belly and occasionally on the back, feet, and tail. There are multiple alleles at this locus including splotch-delayed (Pax3Sp-d, Stock No. 000565), which is similar to splotch but displays caudal rachischisis only. This C57BL/6 congenic strain is also carrying the semidominant naked spontaneous mutation (N).
002879 B6;129-Apobtm2Sgy Apoetm1Unc/J
Cryopreserved - Ready for recovery
Mice homozygous for the Apobtm2Sgy and Apoetm1Unc targeted mutations do not express the apolipoproteins B48 or E, they do express APOB100. Homozygotes are viable and fertile with no overt abnormalities. Compared to the APOB48 APOE deficient mice and the APOE deficient mice, they have the lowest total cholesterol (247mg/dl), lowest LDL cholesterol, and the least extensive Atherosclerotic lesions. The extent of atherosclerosis correlated significantly with plasma cholesterol levels.
020997 B6;129-Arhgap35tm1Jset/AjkJ
Cryopreserved - Ready for recovery
Grlf1 (glucocorticoid receptor DNA binding factor 1) encodes p190 RhoGAP, a member of the Rho family of small GTPases which are critical regulators of actin cytoskeleton organization. p190 RhoGAP is expressed throughout the developing nervous system where it is involved in hippocampal dendritic spine and synapse stability. In this strain a neo cassette replaces part of exon 1, containing the translation initiation site and the GTPase domain, thereby abolishing gene function. Heterozygotes are viable and fertile. Homozygotes are not viable and have abnormalities in fusing the forebrain hemispheres, neural tube closure, forming the optic cup, shaping ventricles, and layering of the cerebral cortex.
003000 B6;129S-Ldlrtm1Her Apobtm2Sgy/J
Cryopreserved - Ready for recovery
This strain expresses only APO-B100 (normally expressed in the liver and yolk sac) and is deficient in low density lipoprotein receptor (Ldlrtm1Her/Ldlrtm1Her).
002221 B6;129S-Twist1tm1Bhr/J
Cryopreserved - Ready for recovery
Homozygotes die at embryonic day 11.5. The most prominent phenotype is a failure of cranial neural tube closure. At embryonic day 8.5 the cranial neural folds are elevated but not fused. At embryonic day 9.5 exencephaly is evident (the cranial neuroepithelium is everted and exposed). There is also abnormal somite morphology and abnormal limb bud development.
004373 B6;129S6-Apaf1tm1Her/J
Cryopreserved - Ready for recovery
Mice that are heterozygous for the targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Most homozygous mutant mice have a perinatal lethal phenotype with severe neuropathology (exencephaly or cranioschesis). Five percent of homozygous null mice survive to weaning age with hydrocephalus, but do not survive much longer. Another five percent survive to adulthood and exhibit hyperactivity. Surviving male homozygotes are infertile. Homozygous female mice are fertile and have litters, but at a reduced frequency. Homozygous male mice are infertile due to massive degeneration of spermatogonia and reduced sperm. At age E9.5 in development neural tube closure defects and thickened neuropithelium appear. No targeted gene product (protein) was immunodetected in homozygous mutant mice. Fibroblast extracts from mutant adult mice do not activate caspase-3. This mutant mouse strain represents a model that may be useful in studies of th .....
For more information please see the full phenotype on the strain data sheet
002877 B6;129S7-Apobtm2Sgy/J
Cryopreserved - Ready for recovery
Mice homozygous for the Apobtm2Sgy targeted mutation express only the APOB100 protein; development is normal and there are no intestinal abnormalities. LDL cholesterol is normal. These homozygoous mice have the lowest HDL cholesterol compared to wildtype and APOB48 expressing mice (B6,129-Apobtm1Sgy/J, Stock No. 002876).
003120 B6;129S7-L1camtm1Sor/J
Cryopreserved - Ready for recovery
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.
000636 B6C3Fe a/a-Lmx1adr-J/J
Cryopreserved - Ready for recovery
Lmx1a encodes a LIM homeodomain (LIM-hd) protein that is expressed in the roof plate along the neuraxis during CNS development. The Lmx1adr-J mutation replaces a conserved cysteine in the LIM1 domain of the protein with a tyrosine (Millonig et al. 2000).

Mice homozygous for Lmx1adr-Jare identifiable at birth by a thin filament extending from the end of the tail, which drops off within a few days, and a short or blunt tail. They may also have a head bleb. When fur develops, there may be a white belly spot. Lmx1adr-J/Lmx1adr-J mice are ataxic and hyperactive and have difficulty righting themselves, and they do not reproduce (Sweet and Wahlsten 1983). They also exhibit circling behavior, are deaf, and have inner ear and vertebral malformations (Manzanares et al. 2000).

Lmx1adr-J homozygotes exhibit defects of three classes of anatomic structures: the hindbrain roof plate, neural crest derived .....
For more information please see the full phenotype on the strain data sheet

000243 B6C3Fe a/a-Wnt1sw/J
Cryopreserved - Ready for recovery
Mice homozygous for the swaying spontaneous mutation (Wnt1sw) sway to one side or the other when attempting to move and may then pivot clockwise or counterclockwise around their rear legs. Homozygous mutant mice display marked ataxia and hypertonia that is probably attributable to malformations of the anterior vermis of the cerebellum and of the colliculi. The cerebellum is divided on the midline by a deep dorsal sagittal fissure extending from the leptomeninges down to the level of the fourth ventricle. The probable cause is failure of the midline fusion of the cerebellum.
000288 B6CBACa Aw-J/A-we a Mafbkr/J
Cryopreserved - Ready for recovery
000553 B6EiC3Sn a/A-Egfrwa2 Wnt3avt/J
Cryopreserved - Ready for recovery
Mice homozygous for the spontaneous waved 2 mutation (Egfrwa2) are recognizable at 2 to 3 days by curly whiskers. The first coat is waved but later coats are not; vibrissae usually remain curled and the guard hairs curved. Some homozygotes have eyelids open at birth. Fertile mutant females have impaired lactation. Mice homozygous for the vestigial tail spontaneous mutation (Wnt3avt) have very short tails, few presacral vertebrae, and abnormal formation of the lumbar vertebrae.
000250 BNT/LeJ
Cryopreserved - Ready for recovery
In the early 1950s, a wild type female from the Namru strain was crossed with a bald hrba/hrba male and one of the pups produced was a male with a bent tail. Pedigree tests revealed the underlying mutation to be semidominant and carried on the X chromosome. The predominant phenotypic trait of kinked, shortened tails results from mis-formed, smaller, and absent tail vertebrae. Heterozygous females have varied expressivity spanning a broad phenotypic range including mice with no apparent phenotype and mice with multiply kinked and shortened tails. Hemizygous males have the highest expressivity; the tail is shortened in some cases to half the normal length and in the most severe cases the kinks in the tail will cause the tail to bend sharply. In males the tail kinks are more common in the distal than the proximal half of the tail. Heterozygous females are fertile, but hemizygous males and homozyous females have decreased viability and fertility. T .....
For more information please see the full phenotype on the strain data sheet
000316 C3H/HeSn-Gpr161vl/J
Cryopreserved - Ready for recovery
001434 C3HeB/FeJ x STX/Le-Mc1rE-so Gli3Xt-J Zeb1Tw/J
Cryopreserved - Ready for recovery
Mice heterozygous for the twirler mutation (Zeb1Tw) display head-shaking and circling behavior but are not deaf. There are morphological abnormalities of the inner ear which consist of irregularities in the outline of the semicircular canals, sometimes amounting to branching, and reduction or absence of otoliths. Moderate astrocytosis in the vestibular nuclei and cerebellar white matter has been reported. Homozygotes have cleft lip and palate or cleft palate only. They die within 24 hours after birth. Viability and fertility are normal except that adults tend to become obese and may then become sterile. Penetrance is incomplete. This strain is also carrying the sombre (Mc1rE-so) and extra toes-Jackson (Gli3St-J) mutations. Extra toes-J heterozygotes have varying numbers of extra digits on preaxial side of feet. Homozygotes die in utero with multiple abnormalities. Excessively large pharyngeal arches and an open neural tube a .....
For more information please see the full phenotype on the strain data sheet
001533 C3HeB/FeJ-Mc1rE-so Gli3Xt-J/J
Cryopreserved - Ready for recovery
Mice heterozygous for the extra toes-J spontaneous mutation (Gli3Xt-J) have varying numbers of extra digits on preaxial side of feet. Homozygous mutant mice die in utero with multiple abnormalities. Excessively large pharyngeal arches and an open neural tube are evident at E9. Homologous to Grieg's cephalopoly-syndactyly, a rare multi-system syndrome in humans. This strain is homozygous for the sombre mutation (Mc1rE-so).
000565 C57BL/6J-Pax3Sp-d/J
Cryopreserved - Ready for recovery
Mice homozygous for the splotch-delayed spontaneous mutation (Pax3Sp-d) have a phenotype that is generally less severe than mice homozygous for the splotch mutation (Pax3Sp, Stock No. 002469). Splotch-delayed homozygous embryos survive to birth, compared to splotch mutant embryos that die at E13 due to neural tube defects. Homozygous splotch-delayed mutant embryos display caudal rachischisis only. Heterozygous splotch-delayed have a white belly spot. Delayed splotch is a point mutation within the paired domain of Pax3. This impairs DNA binding of this domain and also, suprisingly, of the homeodomain, not directly affected in the mutant gene.
006130 CBACa.Cg-ScribCrc/RachJ
Cryopreserved - Ready for recovery
Mice homozygous for this spontaneous mutation develop severe neural tube defects and die at birth. In it's most severe form, the neural tube fails to initiate Closure 1 (craniorachischichisis). Heterozygotes, predominantly males, often exhibit a looping or kinked tail. This strain may used to research neural tube defects.
000092 FL/1Re-KitW/J
Cryopreserved - Ready for recovery
Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes are small at birth and have a transitory siderocytic hypochromic anemia due to defective heme synthesis in fetal but not adult reticulocytes. Fetal erythrocytes have more alpha hemoglobin synthesis than beta hemoglobin synthesis. Very high numbers of siderocytes are found at birth and this decreases during the first few weeks of life and stabilizes at approximately 3 weeks of age with 3% siderocytes, significantly higher than in wildtype adults. Most homozygotes have a belly spot and 1 to 5 flexures in the tail due to vertebral fusions. Vertebral fusions are also found elsewhere in the vertebral column. Fewer than expected homozygotes are generated indicating prenatal death and the postnatal death rate is approximately 4 times normal. A small minority of homozygotes have been .....
For more information please see the full phenotype on the strain data sheet
000023 FL/1ReJ
Cryopreserved - Ready for recovery
Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes are small at birth and have a transitory siderocytic hypochromic anemia due to defective heme synthesis in fetal but not adult reticulocytes. Fetal erythrocytes have more alpha hemoglobin synthesis than beta hemoglobin synthesis. Very high numbers of siderocytes are found at birth and this decreases during the first few weeks of life and stabilizes at approximately 3 weeks of age with 3% siderocytes, significantly higher than in wildtype adults. Most homozygotes have a belly spot and 1 to 5 flexures in the tail due to vertebral fusions. Vertebral fusions are also found elsewhere in the vertebral column. Fewer than expected homozygotes are generated indicating prenatal death and the postnatal death rate is approximately 4 times normal. A small minority of homozygotes have been .....
For more information please see the full phenotype on the strain data sheet
000259 JE/LeJ
Cryopreserved - Ready for recovery
Mice homozygous for the jerker spontaneous mutation (Espnje) show behavior typical of the circling mutants - head-tossing, circling, and hyperactivity. Homozygous mutant mice are deaf from birth and have no detectable stimulus-related cochlear potential at any stage. The abnormal behavior and deafness are associated with postnatal degeneration of the sensory cells of the cochlea and the sacculus and utriculus in homozygotes. The primary influence of the jerker gene appears to be on the apical hair cells, not development of neural structures. Heterozygous jerker mice undergo a similar type of degeneration, but the onset is delayed. Auditory brainstem response is totally absent in homozygotes while heterozygous mice undergo a progressive impairment with age.

Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes ar .....
For more information please see the full phenotype on the strain data sheet
000220 LPT/LeJ
Cryopreserved - Ready for recovery
002979 STOCK Apaf1fog/J
Cryopreserved - Ready for recovery
Mice homozygous for the forebrain overgrowth recessive spontaneous mutation (fog) display forebrain, lumbo-sacral, and facial defects most likely due to excessive growth or cellular proliferation ultimately causing abnormalities in neural tube closure. The phenotypes manifest as head bumps and sacral spina bifida and individual mice can have either or both. Three unique features of the mutant are (1) the growth of telencephalon cells into the surrounding mesenchyme, (2) presence of an encephalocele through the midline cleft in some mutants, and (3) dissociation of the tail defect from the caudal neural tube defect. The fog mutation maps to mouse Chromosome 10 near D10Mit262 and D10Mit230.
001813 STOCK Grhl3ct/J
Cryopreserved - Ready for recovery
013123 STOCK Gt(ROSA)26Sortm6(Gli1)Amc/J
Cryopreserved - Ready for recovery
These RosaGli1Flag c/c mice contain a floxed-neomycin resistance (neo) cassette and polyadenylation signal, cDNA encoding a FLAG-tagged GLI-Kruppel family member (Gli1) gene, an internal ribosome entry site (IRES), and a Venus yellow fluorescent protein (YFP) under control of the ubiquitous Gt(ROSA)26Sor locus. Breeding these mutant mice to mice that express Cre-recombinase will also result in Floxed-neo-stop excision. When these mice are crossed to mice containing Cre-recombinase under direction of an atonal homolog 1 (Math1) promoter, active in dividing granule neuron precursor cells and medulloblastoma tumors, the mice produce Gli1Flag at levels higher than the endogenous protein in the cerebellum. These mice may be useful for understanding Sonic hedgehog signaling and identifying targets of Gli1 action in developing ventral neural tube.
004192 STOCK Mttptm2Sgy Ldlrtm1Her Apobtm2Sgy Tg(Mx1-cre)1Cgn/J
Cryopreserved - Ready for recovery
These mice are homozygous for four different induced mutations. The cumulative result of these mutations is a mouse model in which hypercholesterolemia can be reversed. By themselves, the combined presence of the Ldlrtm1Sgy and Apobtm1Sgy targeted alleles results in mice with a high susceptibility to atherosclerosis and total plasma cholesterol levels of approximately 300 mg/dl. A functional microsomal triglyceride transfer protein gene (Mttp) is essential for establishing a hypercholesterolemic condition. By flanking the Mttp gene with loxP sites and including a Mx1-Cre transgene, it is possible to reduce total plasma cholesterol levels from 300 mg/dl to 30 mg/dl upon induction of the Cre recombinase by administering interferon alpha, interferon beta, or synthetic double-stranded RNA. This unique model is useful in research related to the mechanisms and events of atherosclerotic reversal. Mice homozygous for the targeted .....
For more information please see the full phenotype on the strain data sheet
002902 STOCK Pax3Sp Mlphln/J
Cryopreserved - Ready for recovery
014645 STOCK Sec24bY613X/J
Cryopreserved - Ready for recovery
Mice heterozygous for this ENU-induced mutation (Sec24bY613X), are viable and fertile, although the donating investigator reports that 33% of homozygous mice are dead or dying by E18.5. Sec24b is a cargo-sorting member of the core complex of the COPII endoplasmic reticulum (ER)-Golgi transport vesicle, and is critical for neural tube closure. These mice contain a premature stop codon in exon 9 of the Sec24 related gene family, member B (Sec24b) gene. Sec24bY613X homozygotes develop craniorachischisis, a fully open neural tube from the midbrain-hindbrain boundary to the most caudal end of the neural tube. These mice exhibit deficits in convergent extension and other planar cell polarity phenotypes. At E18.5, 45% of embryos exhibit omphalocele and 99% exhibit eyelid fusion failure. Also, outer and inner cochlear hair cells periodically fall out of phase and are abnormally aligned. These mutant mice may be useful in studying planar cel .....
For more information please see the full phenotype on the strain data sheet
003318 STOCK Shhtm1Amc/J
Cryopreserved - Ready for recovery
Mice homozygous for the Shhtm1Amc targeted mutation display early defects in the establishment and maintenance of midline structures. These defects result from the critical role the Sonic hedgehog (Shh) gene plays in the patterning patterning of vertebrate embryonic tissues, including the brain and spinal cord, the axial skeleton and the limbs. Defects are also observed in all tissues, confirming the proposed role of SHH proteins as an extracellular signal required for the tissue-organizing properties of several vertebrate patterning centers.

When bred to a strain with loxP sites inserted into the same targeted allele (Stock No. 004293) and a strain expressing Cre recombinase in the skin and dental epithelium (Stock No. 004782), this mutant mouse strain may be useful in studies of hedgehog signalling and cell proliferation in the dental e .....
For more information please see the full phenotype on the strain data sheet

003119 STOCK Sp4tm1Ssp/J
Cryopreserved - Ready for recovery
001814 STOCK Tc/J
Cryopreserved - Ready for recovery
000312 STOCK stb + a/+ Fignfi a/J
Cryopreserved - Ready for recovery
Mice homozygous for the fidget spontaneous mutation (Fignfi) toss their heads from side to side and tend to run in circles. Homozygous fidgit mice are hypersensitive to sound in early life, but later lose hearing ability. Corneal lesions are common, and hind foot polydactylism occurs. The bony labyrinth is quite defective. Other abnormalities including small eyes, absence of lachrymal glands, dislocation of the hip, and displaced parafloccular lobes of the cerebellum. Viability of homozygotes is usually less than normal and fertility is poor. The STOCK is also carrying the stubby spontaneous mutation (stb). Homozygous stubby mice are recognizable at 4 or 5 days by a domed head and thick short tail. Adult stubby mice have shorter heads, bodies, and legs compared to wildtype mice. Most females are fertile but males do not breed. Male mice do produce normal numbers of motile sperm. Cartilage histology is within normal limits, but chondrogenesis stops earlier than .....
For more information please see the full phenotype on the strain data sheet
001874 STOCK tw82 Itpr3tf/J
Cryopreserved - Ready for recovery
000791 WB.Cg-f/J
Cryopreserved - Ready for recovery
Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes are small at birth and have a transitory siderocytic hypochromic anemia due to defective heme synthesis in fetal but not adult reticulocytes. Fetal erythrocytes have more alpha hemoglobin synthesis than beta hemoglobin synthesis. Very high numbers of siderocytes are found at birth and this decreases during the first few weeks of life and stabilizes at approximately 3 weeks of age with 3% siderocytes, significantly higher than in wildtype adults. Most homozygotes have a belly spot and 1 to 5 flexures in the tail due to vertebral fusions. Vertebral fusions are also found elsewhere in the vertebral column. Fewer than expected homozygotes are generated indicating prenatal death and the postnatal death rate is approximately 4 times normal. A small minority of homozygotes have been .....
For more information please see the full phenotype on the strain data sheet

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Stock
Number
Strain Name
 
Strain Description
Standard Supply
000317STOCK a/a Egfrwa2/J
On Hold
Mice homozygous mice for the waved 2 spontaneous mutation (Egfrwa2) are recognizable at 2 to 3 days by curly whiskers. The first coat is waved but later coats are not; vibrissae usually remain curled and the guard hairs curved. Some homozygotes have eyelids open at birth. Fertile mutant females have impaired lactation.

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