Search Criteria: Research Area is "Developmental Biology Research: Craniofacial and Palate Defects"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 000646 | A/J | Level 2 |
| Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A inbred strain is used widely used in cancer and immunology research. It is highly susceptible to cortisone-induced congenital cleft palate. It has a high incidence of spontaneous lung adenomas, and lung tumors readily develop in response to carcinogens. A high percentage of mammary adenocarcinomas (a large proportion of acinar-type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains. A/J mice fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid, and 15% fat) fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 000668, C57BR/c
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| 004337 | 129(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 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. | ||
| 004293 | 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
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| 007199 | 129S-Sgpl1Gt(ROSA)78Sor/J | Repository- Live |
| Mice homozygous for this mutant allele have reduced size and weight gains after birth and do not survive past 8 weeks of age. Homozygotes occur at a lower than Mendelian ratio (19%) from heterozygote X heterozygote crosses. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Beta-galactosidase staining pattern mimics the endogenous gene expression pattern in adult intestinal epithelial cells. Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At 6 weeks of age, mutant mice are anemic (low hemoglobin concentration, reduced red blood cell count, low hematocrit). Mutants exhibit polychromasia (abnormally high number of immature blood cells), kidney defects (blood urea nitrogen level abnormally high, kidney size smaller than wildtype, swollen blood filled glomeruli, reduced number of vascular smooth muscle cells) and abnormalities in palate bone fusion. Homozygotes are infertile. Heterozygote
..... For more information please see the full descriiption on the strain data sheet | ||
| 000645 | A/HeJ | Repository- Live |
| Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A inbred strain is used widely used in cancer and immunology research. It is highly susceptible to induction of congenital cleft palate by cortisone. It has a high incidence of spontaneous lung adenomas and lung tumors readily develop in response to carcinogens. High percentage of mammary adenocarcinomas (a large proportion acinar type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains. A small percent (4%) of nonproductive males are hermaphrodites. An additional 17% of nonproductive males have abnormally small testes containing no sperm. | ||
| 000647 | A/WySnJ | Repository- Live |
| Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A inbred strain is used widely used in cancer and immunology research. It is highly susceptible to induction of congenital cleft palate by cortisone. It has a high incidence of spontaneous lung adenomas and lung tumors readily develop in response to carcinogens. High percentage of mammary adenocarcinomas (a large proportion acinar type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains. Unlike A/J mice, A/WySnJ mice carry a spontaneous mutation in Tnfrsf13c and exhibit a significant loss of mature B cells (Miller, et al., 1991, Lentz et al., 1996, Shulga-Morskaya et al., 2004). | ||
| 005717 | B6(NOD) H2g7-Sostdc1shk/J | Repository- Live |
| 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 descriiption on the strain data sheet | ||
| 005981 | B6.129S7-Rai1tm1Jrl/J | Repository- Live |
| Mice are albino. Heterozygous mice are viable and fertile and weigh slightly less than wildtype at 0-2 weeks of age. RT-PCR shows a blunted N-terminal product in kidney tissues that does not contain the two nuclear localization signals (NLS) or zinc finger like plant homeo domain (PHD). Heterozygous embryos have differential tissue expression of lacZ during development, faithfully recapitulating the expression pattern of Rai1. Less than 5% of heterozygous mice exhibit polydactyly. While noticeably smaller at 4-7 weeks, heterozygotes are significantly obese by 20-23 weeks. 7-18% of heterozygotes have craniofacial defects (broader and shorter nasal bone and lateral bending of the snout). The vast majority of homozygotes are embryonic lethal, with death occurring after implantation but before 15.5 days post coitum (during gastrulation and organogenesis). All homozygotes surviving to birth exhibit growth retardation and premature death with most dying before wean. Homozygous mice ha
..... For more information please see the full descriiption on the strain data sheet | ||
| 004088 | B6.Cg-Foxp3sf/J | Repository- Live |
| Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. Phenotypes associated with these mice include runting, scaly, crusty skin on the eyelids, ears and tails, dermal thickening, squinted eyes, cachexia, reddening and swelling of the genital papilla, and small testicles that are retained in the abdominal cavity. This disorder, which parallels X-linked autoimmunity-allergic disregulation syndrome (XLAAD) in humans, results in Coombs' test-positive anemia, hypergammaglobulinemia, a small, thin thymus, and lymphohistiocytic proliferation in the skin and lymphoid organs, with splenomegaly, lymphadenomegaly, and hepatomegaly. Foxp3sf/Y males generally die by 16-25 days of age. Transgenic expression of Foxp3 prevents scurfy disease in Foxp3sf/Y mice. Neonatal thymectomy of scurfy males ameliorates disease and increases lifespan; athymic nude Foxp3sf/Y mice do not develop scurfy
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| 006229 | B6.Cg-Tg(DRE-lacZ)2Gswz/J | Repository- Live |
| Hemizygous mice are viable, fertile, normal in size, and do not display any behavioral abnormalities. Following adult or in utero exposure with xenobiotic ligands (including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and polychlorinated biphenyls (PCBs)), lacZ expression is induced in tissues targeted by the toxic compounds; for example, embryonic tissues expressing beta-galactosidase following TCDD treatment in utero include hard and soft palates, genital tubercle, certain facial regions, shoulder, and other tissues). These mice may be useful in studies of toxicology, teratogenic and xenobiotic processes, Per-Arnt-Sim transcription factors, cleft-palate, and as a reporter strain to indicate the temporal and spatial context of transcriptionally active aryl hydrocarbon receptors following agonist exposure in vivo. | ||
| 006904 | B6;129-Msctm1Eno/J | Repository- Live |
| Mice homozygous for this MyoR mutant allele are viable and fertile with no obvious abnormalities. These mice may be useful in studying muscle development, specifically craniofacial muscles. For example, when these mice are bred with capsulin-mutant mice, the resulting double mutant offspring have significant abnormalities in craniofacial (and other) muscle development and MyoD-family transcription factor gene expression. 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. | ||
| 007204 | B6;129S4-2610005L07RikGt(ROSA)73Sor/J | Repository- Live |
| Mice homozygous for this mutant allele (called BC058969 in the primary publication) are viable and fertile, with greater than 50% embryonic lethality observed in homozygous embryos. Homozygotes occur at a lower than Mendelian ratio (9%) from heterozygote x heterozygote crosses. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Homozygotes exhibit defects that affect the same cell types and processes as those controlled by the platelet-derived growth factor (PDGF) pathway, including vasculature, kidney, and skeletal defects (sternum and calvarial bones). Notably, 100% incidence of calvarial bones defects is reported. Additionally, homozygotes are reported to have low β-galactosidase activity; in situ hybridization or other sensitive methods may be necessary to detect expression of the lacZ-neo reporter fusion gene. These BC058969-mutant (2610005L07Rik-mutant) mice may be useful in studying cellular signal
..... For more information please see the full descriiption on the strain data sheet | ||
| 007200 | B6;129S4-Arid5bGt(ROSA)75Sor/J | Repository- Live |
| Mice homozygous for this mutant allele have reduced size and weight gains after birth, occur at lower than Mendelian ratio (16%) and 46% die within 3 weeks of age. Homozygotes are fertile when they survive to adulthood. Heterozygotes are viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Homozygotes exhibit kidney defects (abnormally high blood urea nitrogen level, mutant kidney size smaller than wildtype, swollen blood filled glomeruli, reduced number of vascular smooth muscle cells in glomeruli), and abnormalities in palate bone fusion. These Arid5b-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation. | ||
| 007206 | B6;129S4-TiparpGt(ROSA)79Sor/J | Repository- Live |
| Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At 6 weeks of age, mice are anemic (low hemoglobin concentration, red blood cell count, hematocrit). These mice also exhibit polychromasia (abnormally high number of immature blood cells); kidney defects (blood urea nitrogen level abnormally high, kidney size smaller than wildtype, swollen blood filled, degraded glomeruli are often observed, increased number of vascular smooth muscle cells partially filling the glomeruli space); and abnormalities in palate bone fusion. Homozygotes occur at lower than Mendelian ratio (22%), and 32% die by age 2 week. Heterozygotes are viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. These Tiparp-mutant mice may be useful in studying kidney development, vascular development, hematopoiesis and cellular signaling during development and in adult mice; specifically receptor tyrosine
..... For more information please see the full descriiption on the strain data sheet | ||
| 007202 | B6;129S4-Zfp826Gt(ROSA)76Sor/J | Repository- Live |
| At age E11.5 to E18.5, homozygous embryos exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At six weeks of age, mice are anemic (low hemoglobin concentration, red blood cell count, hematocrit). These mice also exhibit polychromasia (abnormally high number of immature blood cells); kidney defects (abnormally high blood urea nitrogen level, kidney size smaller than wild-type, swollen blood filled glomeruli, reduced number of vascular smooth muscle cells in glomeruli); abnormalities in palate bone fusion and abnormal neural crest derived and thoracic skeleton development. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Homozygotes occur at lower than Mendelian ratio (18%) and 8% die by age one week. Surviving homozygotes and heterozygotes are viable and fertile. These Zfp826 (BC055757)-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (R
..... For more information please see the full descriiption on the strain data sheet | ||
| 004758 | B6;129S7-Wnt5atm1Amc/J | Repository- Live |
| Homozygous null mice have a perinatal lethal phenotype and do not survive long after birth due to respiratory failure. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by immunohistochemical analysis in homozygotes. Homozygous 17.5 to 18.5 embryonic day old embryos exhibit severe shortening in all outgrowing axes of the body and limbs with loss of distal structures (absence of tail, limb digits and genital tubercle), and truncated facial features. Newborn homozygous mice succumb to asphyxia due to abnormal lung development and display shortened trachea, overexpansion of the distal airways and impaired capillary/alveolar coupling. This mutant mouse strain may be useful in studies of distal outgrowth of internal organs and organization of morphogenesis in development. | ||
| 000636 | B6C3Fe a/a-Lmx1adr-J/J | Repository- Live |
| 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
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| 004476 | C3H/HeJ-snol/J | Repository- Live |
| The snol homozygous mutant phenotype includes a short nose, odd face and body shape, and kinked tail. Most mutants also get malocclusion and two homozygous mutants tested at 49 days of age exhibited intermediate hearing loss ( about 25 dB above normal). The odd shape of the face can be used to distinguish the Homozygotes by 14 days of age. snol has been mapped to Chromosome 4. The most likely gene order places the mutation between D4Mit12 and D4Mit203 in 92 tested meioses. A short nosed mutation, snubnose (sno), maps in this location, but could not be tested for allelism because it is believed to be extinct. The spina bifida occulta reported in sno homozygotes is not seen in snol homozygotes. | ||
| 004246 | C57BL/6J-sbse/J | Repository- Live |
| 008343 | FVB.Cg-Hydinhy3/MlrJ | Repository- Live |
| Mice homozygous for the hydrocephalus 3 spontaneous mutation of the hydrocephalus inducing gene (Hydinhy3) are usually identifiable at three to five days. Those with frank hydrocephalus develop hydrocephalus with early perinatal onset, and most animals die by three to five weeks of age. Penetrance is incomplete. Hydrocephalus is associated with a central pair defect impairing ciliary motility and fluid transport in the brain. Hydin-deficiency also impairs
the beat pattern of ependymal and tracheal cilia. These Hydinhy3 mutant mice may be useful in neurological and developmental studies.
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
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| 000644 | SEA/GnJ | Repository- Live |
| 000274 | TSJ/LeJ | Repository- Live |
| 007209 | 129S-Schip1Gt(ROSA)77Sor/J | Repository-Cryopreserved |
| Homozygotes occur at lower than Mendelian ratio (19%), and 20% die by age 1 week. Heterozygotes viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Homozygotes exhibit abnormalities in neural crest-derived and thoracic skeleton development, and palate bone fusion. These Schip1-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation. | ||
| 003485 | A/J-frg/J | Repository-Cryopreserved |
| Mice homozygous for the froggy mutation have a smaller body size and a shortened face with wide set eyes. | ||
| 004235 | B6(AKR)-Sofa/J | Repository-Cryopreserved |
| 007448 | B6.129-Akap6tm1Jsco/38J | Repository-Cryopreserved |
| 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. | ||
| 005709 | B6.129-Skitm1Cco/J | Repository-Cryopreserved |
| 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 descriiption on the strain data sheet | ||
| 002619 | B6.129-Tgfb3tm1Doe/J | Repository-Cryopreserved |
| Mice homozygous for the Tgfb3tm1Doe mutation are not viable. Mice exhibit cleft palate and possibly developmental defects in the lung. | ||
| 002612 | B6.129S2-Bmp4tm1Blh/J | Repository-Cryopreserved |
| Mice homozygous for the Bmp4tm1Blh targeted mutation mutation die early in embryogenesis. Fifteen to twenty percent of heterozygous mice show developmental defects including polydactyly, craniofacial defects, and cystic kidneys. Heterozygotes have also been reported to show eye abnormalities. | ||
| 004069 | B6.129S6-Crebbptm1Dli/J | Repository-Cryopreserved |
| 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. | ||
| 005535 | B6.129S7-Del(11Cops3-Zfp179)1Jrl/J | Repository-Cryopreserved |
| These mutant mice possess an engineered deletion spanning approximately 3 Mb on mouse Chromosome 11. The region involved encompasses a chromosomal segement that shares conserved synteny with the Smith-Magenis syndrome (SMS) critical interval on human Chromosome 17. Mice carrying one copy of the deletion prove to be viable while mice homozygous for the deletion are embryonic lethal. Heterozygous males suffer from reduced fertility, exhibiting reduced sperm counts and an increase in sperm structural abnormalities. Mutant mice weigh less than their wild type littermates at birth but rapidly gain weight such that by 4 months of age, they exceed wild type weight and eventually become obese (60 grams by 8 months of age). Mutant mice exhibit craniofacial abnormalities characterized by overall shorter skulls with broader, shorter snouts and nasal bones. Mutants also produce abnormal electroencephalograms (EEG) with tonic clonic-type seizures being observed in 22% of the mice tested. Behavioral
..... For more information please see the full descriiption on the strain data sheet | ||
| 004202 | B6.C3 Pde6brd1 Hps4le/+ +-Lmx1adr-8J/J | Repository-Cryopreserved |
| 001271 | B6.RBF-Nek1kat/J | Repository-Cryopreserved |
| The phenotype associated with the Nek1kat-2J allele is more severe than that of the Nek1kat allele. Mice homozygous for Nek1kat-2J all die before one year of age, a third of those that survive weaning die suddenly before 100 days of age, and the reported median survival age is 211 days. Mice homozygous for Nek1kat also have a shortened life expectancy with high pre-weaning mortality and a reported median survival of 286 days, but 22% were found to survive beyond 1 year. Both mutants are runted and have blunted noses with olfactory bulbs that are approximately half the normal size and lack most of the glomerular and external granular layers. In the brain there is dilation of the lateral and third ventricles, cerebral aqueduct and fourth ventricle along with large, fluid-filled cysts in the choroid plexus. Hydrocephalus occurs. Normochromic normocytic anemia is found and is more pronounced in Nek1Kat-2J
..... For more information please see the full descriiption on the strain data sheet | ||
| 006382 | B6;129-Casktm1Sud/J | Repository-Cryopreserved |
| Homozygous floxed mice are viable and fertile, but females do not thrive. The body size of mutants is significantly smaller than littermate controls and they exhibit a slightly increased mortality. Knock-in mice are hypomorphs and protein is expressed at less than 30% of normal levels. Crossing of the floxed mutants with mice expressing cre recombinase in the male germline excises the floxed exon and a neomycin resistance gene cassette to create a complete knockout of the gene. Knockout homozygotes die within a few hours of birth. They exhibit a partially penetrant cleft palate syndrome and increased apoptosis in the thalamus, but display no other major developmental changes or deficits in basic electrical properties of their neurons.
When bred to a strain expressing Cre recombinase in the male germline (see Stock No. 003328 or 007252 for example), this mutant mouse str
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| 007947 | B6;129P2-He/J | Repository-Cryopreserved |
| 007208 | B6;129S4-Axud1Gt(ROSA)80Sor/J | Repository-Cryopreserved |
| Mice homozygous for this Axud1-mutant allele are viable and fertile, with some incidence of perinatal lethality before two weeks of age (the Donating Investigator reports 18% of homozygotes die by two weeks of age). Homozygotes have abnormalities in palate bone fusion. Homozygotes exhibit defects that affect the same cell types and processes as those controlled by the platelet-derived growth factor (PDGF) pathway, including vasculature, kidney, and skeletal defects. These Axud1-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation. | ||
| 007207 | B6;129S4-Zfp640Gt(ROSA)81Sor/J | Repository-Cryopreserved |
| Mice homozygous for this Zfp640-mutant allele are viable and fertile, with abnormalities in palate bone fusion and increased weight gain observed only in males after adolescence. Homozygotes exhibit defects that affect the same cell types and processes as those controlled by the platelet-derived growth factor (PDGF) pathway, including vasculature, kidney, and skeletal defects. Additionally, homozygotes are reported to have low β-galactosidase activity; in situ hybridization or other sensitive methods may be necessary to detect expression of the lacZ-neo reporter fusion gene. These Zfp640-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation. | ||
| 002788 | B6;129S7-Fsttm1Zuk/J | Repository-Cryopreserved |
| Homozygous mice die within hours after birth due to a failure to breathe. They are smaller in size than normal wildtype siblings and show craniofacial, musculoskeletal, and skin defects. | ||
| 002990 | B6;129S7-Inhbatm1Zuk/J | Repository-Cryopreserved |
| Homozygous mice die within 24 hours of birth. They show craniofacial defects including a cleft palate. | ||
| 000221 | B6C3Fe a/a-Alx4lst-J/J | Repository-Cryopreserved |
| 001430 | B6C3Fe a/a-Ptch1mes/J | Repository-Cryopreserved |
| Mice homozygous for the mesenchymal dysplasia spontaneous mutation (mes) have a shortened face, wide set eyes, excessive skin, belly spot, kinked tail, preaxial polydactyly, and thickened foot pads. Homozygous mutant mice also display mineralization of tendons and multiple skeletal defects. Both sexes are infertile. Male mice have cryptorchid testes. | ||
| 000515 | B6CBACa Aw-J/A-SfnEr/J | Repository-Cryopreserved |
| 007552 | B6SJL-Chrdtm1Emdr/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation die at birth. They display an extensive array of head and neck congenital malformations simlar to the DiGeorge and Velo-Cardio-Facial syndromes. At low penetrance, they show early lethality and a ventralized gastrulation phenotype. No transcription was found by in situ hybridization of gastrulation phase embryos. Some heterozygotes display a circling behavior. | ||
| 007556 | B6SJL-Gsctm1Pgr/J | Repository-Cryopreserved |
| Homozyous mutant mice are small and die within 24 hours of birth and display defects of the lower mandible and associated musculature, the inner ear and external audiatory meatus. | ||
| 001434 | C3HeB/FeJ x STX/Le-Mc1rE-so Gli3Xt-J Tw/J | Repository-Cryopreserved |
| Mice heterozygous for the twirler mutation (Tw) 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 are evident at E
..... For more information please see the full descriiption on the strain data sheet | ||
| 005322 | C57BL/6J-Gusbmps-3J/J | Repository-Cryopreserved |
| 002854 | C57BL/6J-Nek1kat-2J/J | Repository-Cryopreserved |
| The phenotype associated with the Nek1kat-2J allele is more severe than that of the Nek1kat allele. Mice homozygous for Nek1kat-2J all die before one year of age, a third of those that survive weaning die suddenly before 100 days of age, and the reported median survival age is 211 days. Mice homozygous for Nek1kat also have a shortened life expectancy with high pre-weaning mortality and a reported median survival of 286 days, but 22% were found to survive beyond 1 year. Both mutants are runted and have blunted noses with olfactory bulbs that are approximately half the normal size and lack most of the glomerular and external granular layers. In the brain there is dilation of the lateral and third ventricles, cerebral aqueduct and fourth ventricle along with large, fluid-filled cysts in the choroid plexus. Hydrocephalus occurs. Normochromic normocytic anemia is found and is more pronounced in Nek1Kat-2J
..... For more information please see the full descriiption on the strain data sheet | ||
| 000118 | C57BL/6J-Ph/J | Repository-Cryopreserved |
| 000293 | CHMU/LeJ | Repository-Cryopreserved |
| Mice homozygous for the congenital hydrocephalus (Foxc1ch) spontaneous mutation die at birth, probably from inability to breathe. Homozygous mutant mice have bulging hemorrhagic cerebral hemispheres and open eyelids, urogenital abnormalities, and severely abnormal skull, cervical vertebrae, sternum, laryngeal cartilages, and hyoid bone. The hydrocephalus may trace to lack of formation of subarachnoid space, which is first detectable in 11-day embryos. Most of the defects in the head region are probably secondary to the severe displacements created by the hydrocephalus. Mice homozygous for the muted spontaneous mutation (Mutedmu), maintained in repulsion with congenital hydrocephalus, have light eyes at birth and their fur is a muted brown shade, often with white underfur. Some have a balance defect, similar to that of pallid (Pldnpa). Homozygous mutant mice show head-tilting and loss of postural reflexes, due to absence of otoliths
..... For more information please see the full descriiption on the strain data sheet | ||
| 000252 | DC/LeJ | Repository-Cryopreserved |
| Mice heterozygous for the semidominant dancer mutation exhibit head tossing and circling behavior. Heterozygotes are not deaf, but have defects in the vestibular region (Wenngren et al., 1989). Homozygotes die at birth with cleft lip and cleft palate (Deol et al., 1966). Strain background influences cleft lip/palate expression in heterozygotes (Trasler et al., 1982). Positional cloning of Dc revealed a 3.3 kb insertion of the Tebp gene into the first intron of Tbx10. The insertion causes ectopic expression of a Tebp-Tbx10 chimeric transcript (Bush et al., 2004). | ||
| 005057 | FVB.129-Kcnj2tm1Swz/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation have a complete cleft of the secondary palate and die within 12 hours of birth. Heterozygotes 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 Northern blot analysis of cardiac tissue or Southern blot analysis. Inwardly rectifying potassium ion currents are absent in cerebral artery myocytes and cardiac ventribular myocytes isolated from homozygote neonates. Elevated external potassium ion concentrations do not dilate isolated neonatal cerebral arteries. Homozygotes exhibit altered electrocardiogram profiles indicative of reduced heart rate and bradycardia. This mutant mouse strain may be useful in studies of potassium ion dependent vasodilation, cardiac arrythmia such as Anderson syndrome, cleft palate and developmental bone malformation. | ||
| 000572 | JIGR/DnJ | Repository-Cryopreserved |
| JIGR/Dn is maintained with jittery (Atcayji) and grizzled (gr) in repulsion.
Atcayji 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 approxi
..... | ||
| 000265 | MY/HuLeJ | Repository-Cryopreserved |
| 001747 | STOCK Oca2p-d/Oca2p-cp/J | Repository-Cryopreserved |
| Mice homozygous for Oca2p-d (dark pink-eye) are born with lightly pigmented eyes, darker than those of Oca2p/Oca2p mice, which darken by weaning and a coat color "considerably darker than that of Oca2p/Oca2p mice, somewhat resembling that of brown [Tyrp1b/Tyrp1b] mice"; both sexes are fertile (Gardner et al. 1977, Lyon et al. 1992). A normal-sized Oca2p transcript is present in eyes of Oca2p-d/Oca2p-d mice (Gardner et al. 1992), and Southern blot analysis revealed no gross alteration of the Oca2p gene (Gardner et al. 1992, Lyon et al. 1992); thus, the molecular nature of the defect is unknown. Most Oca2p-cp (p-cleft palate, formerly p11H) homozygotes die soon after birth with cleft palate; the few that survive to adulthood exhibit significant dilution of coat co
..... For more information please see the full descriiption on the strain data sheet | ||
| 003318 | STOCK Shhtm1Amc/J | Repository-Cryopreserved |
| 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
..... | ||
| 000279 | STOCK gr +/+ Ap3d1mh/J | Repository-Cryopreserved |
| Mice homozygous for the mocha spontaneous mutation (Ap3d1mh) have increased perinatal mortality. They are recognizable at birth by the absence of visible pigment in the eyes, which darken to deep red in adults. The hairs have considerably smaller and fewer melanin granules than normal. Behavior is abnormal, characterized by hyperactivity, tilted heads, and in some the inability to swim. All homozygotes show degenerative changes in the organ of Corti, stria vascularis, and spiral ganglion, and most show abnormalities of the otoliths in the saccule and utricle. This degeneration can be lessened by the administration of supplemental manganese or, to a lesser degree, zinc to the dam during pregnancy. Evoked auditory brainstem responses appear normal in young homozygotes, but decrease with age coincident with the cochlear degeneration with no response detected after six months of age. At three months of age, mice homozygous for the Ap3d1mh allele have si
..... For more information please see the full descriiption on the strain data sheet | ||
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How to Register Interest
Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.View a Data sheet for New Strains Under Development
Select the strain name to link to the strain data sheet.
New Strains Under DevelopmentThe Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion. Strains "Under Development" fall into two categories depending on the anticipated demand from the scientific community.
- Receive periodic updates on the status of the colony UNDER DEVELOPMENT
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It is VERY IMPORTANT that you register interest in strains Under Development. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain Under Development. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.
- Strains that will be made available from a live distribution colony at The Jackson Laboratory.
These strains are designated as: "Under Development for Distribution Colony"- Strains that will be made available through the Cryopreservation Repository.
These strains are designated as: "Under Development for Cryopreservation Repository"
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