Search Criteria: Research Area is "Developmental Biology Research: Mesodermal Defects"
New Strains Awaiting Transfer from the Donor
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 016222 | B6.129S(Cg)-Id2tm1.1(cre/ERT2)Blh/ZhuJ | Repository- Live |
| The Id2-CreERT2 knockin allele was designed to both abolish inhibitor of DNA binding 2 (Id2) gene function and express CreERT2 fusion protein from the Id2 promoter/enhancer elements. Cre-ERT2 fusion gene activity is inducible and can be observed following tamoxifen administration. As such, when Id2-CreERT2 knockin mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Id2-expressing cells of the offspring.
No mRNA or protein expression from the Id2-CreERT2 allele is observed. The donating investigator reports that homozygous mice are runted with defective lung alveolarization. Other organ systems have not been evaluated. However, Id2-CreERT2 homozygotes may be expected to exhibit the same phenotype as mice homozygous for other null mutations of this gene (including postnatal lethality and defects of the immune system, digestive tract, ..... | ||
| 003755 | B6.129S4-Meox2tm1(cre)Sor/J | Repository- Live |
| This strain expresses Cre recombinase under the control of the endogenous Meox2 promoter. Expression of Cre recombinase is observed in epiblast-derived tissues as early as embryonic day 5. The insertion creates a null allele for the Meox2 gene. Homozygous mice are viable on this background but exhibit an overall reduction in muscle mass and the absence of specific muscles resulting in abnormal limb posture and reduced motility. This phenotype is variable. As many as 80% of homozygotes are severely affected, fail to thrive and die before weaning. Some homozygotes (10%) exhibit clefting of the secondary palate. These mice can be utilized as a deleter strain for loxP flanked DNA and provide an alternative to tetraploid embryo analysis. | ||
| 008712 | B6.129X1-Twist2tm1.1(cre)Dor/J | Repository- Live |
| Dermo1-cre (Twist2-cre) mutant mice harbor a Cre recombinase "knock-in" allele that also abolishes endogenous Twist2 gene function. Heterozygotes are viable and fertile, while homozygotes (twist-2-/-) die a few days after birth. Under control of the upstream promoter/enhancer elements, cre expression is observed in a pattern consistent with the wildtype gene; Cre recombinase activity is reported in mesoderm as early as embryonic day 9.5, in mesodermal tissues such as branchial arches and somites, and in condensed mesenchyme-derived chondrocytes and osteoblasts. When heterozygotes are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequences in Dermo1-expressing tissues of the offspring. Homozygous mice exhibit elevated expression of proinflammatory cytokines resulting in perinatal death from cachexia (wasting), as well as progressive growth retardation, impaired movement, th ..... For more information please see the full phenotype on the strain data sheet | ||
| 014125 | B6;129-Flnctm1Lmk/J | Repository- Live |
| The Flnc Δ41-48 mutant allele has the last eight exons (exons 41-48) of the filamin C (FLNc) locus deleted. The deleted region encodes the last five filamin-like repeats (including the dimerization domain) and the Hinge 2 domain of FLNc. As such, the Flnc Δ41-48 allele expresses a truncated mRNA at reduced levels compared to the wildtype allele in limb muscle and heart tissues. Western blot analysis on limb muscle protein lysates shows that the Flnc Δ41-48 allele expresses a truncated protein at very low levels. Heterozygous mice are viable and fertile with no reported abnormalities. Mice homozygous for the Flnc Δ41-48 allele die at birth. At embryonic day (E)18.5, homozygous mice born via Cesarean section are able to take several short breaths but exhibit respiratory distress (failure to inflate lungs) and die shortly thereafter. While the hearts of the homozygotes appear normal and unaffected, skeletal muscles exhibit severe abnor ..... For more information please see the full phenotype on the strain data sheet | ||
| 016224 | B6.129S(Cg)-Id2tm2.1Blh/ZhuJ | Under Development - Now Accepting Orders |
| The Id2-EGFP knockin allele was designed to both abolish inhibitor of DNA binding 2 (Id2) gene function and express enhanced green fluorescent protein (eGFP) from the Id2 promoter/enhancer elements. No mRNA or protein expression from the Id2-eGFP allele is observed. The donating investigator reports that homozygote mice mice are runted with defective lung alveolarization. Other organ systems have not been evaluated. However, Id2-eGFP homozygotes may be expected to exhibit the same phenotype as mice homozygous for other null mutations of this gene (including postnatal lethality and defects of the immune system, digestive tract, kidneys, adipose tissue and mammary gland development). The donating investigator also reports eGFP expression recapitulates the endogenous Id2 expression pattern. In the lungs, immunohistochemical detection of eGFP recapitulates the epithelial expression of the endogenous gene (distal tip lung epithelial multipotent precursor cells of the ..... For more information please see the full phenotype on the strain data sheet | ||
| 016878 | B6;129S4-Bmp4tm1Jfm/J | Under Development - Now Accepting Orders |
| Mice homozygous for this Bmp4floxneo allele have loxP sites flanking exon 4 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have the sequences encoding the endogenous mature peptide deleted in the cre-expressing tissues resulting in a null allele. Mice homozygous for the Bmp4floxneo allele are viable and fertile. These mutant mice may be useful in generating conditional mutations for studying the role of Bmp4 in bone morphogenetic protein signaling pathways, bone biology, cardiovascular biology, and cancer (Bmp4 misregulation is associated with cancer cell motility/invasiveness and epithelial-to-mesenchymal transition/transformation [EMT]).
For example, when crossed to a strain expressing Cre recombinase in early limb bud mesenchyme and in a subset of craniofacial mesenchyme (see Stock No. 005584), this mutant mouse ..... | ||
| 017981 | STOCK Tg(Hoxb6-cre)Mku/J | Under Development - Now Accepting Orders |
| These mice express Cre recombinase under the control of the mouse homeobox B6 (Hoxb6) lateral plate mesoderm (LPM) enhancer region. HOXB6 is a transcription factor that regulates anterior-posterior axis positioning during development. Hoxb6-Cre is expressed throughout the lateral plate mesoderm at E8.5, in mesoderm of the hindlimb bud at E9.5, and in the entire hindlimb by E11.5. In the forelimb, Cre activity is detected at the posterior end during limb initiation and then extends anterior until nearly the entire limb bud is positive by E11.5. Homozygotes are viable and fertile. When crossed with a strain containing a loxP site-flanked sequence, Cre-mediated recombination results in deletion of the flanked sequence in Cre-expressing tissues of the offspring.
For example, when bred to a strain expressing a floxed-fibroblast growth factor receptor 1 (Fgfr1) gene, the resulting mice exhibit malformed hindlimbs and abnormal posterior portions of the fo ..... | ||
| 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. | ||
| 002274 | B6.129S-Itga5tm1Hyn/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 002475 | B6.129S1-Myf6tm1Wb/J | Cryopreserved - Ready for recovery |
| 009387 | B6.129S1-Osr1tm1Jian/J | Cryopreserved - Ready for recovery |
| The Osr1tm1Jian (Odd1-LacZ) mutation abolishes endogenous gene function and expresses a β-galactosidase fusion protein (fused in-frame with the N-terminal 16 amino acid residues of the endogenous protein). Under control of the upstream promoter/enhancer elements, lacZ expression is directed to the same tissues as the wild-type gene (for example, β-galactosidase expression during embryogenesis is detected at E7.5 in the intermediate mesoderm, is expanded to the gut endoderm, lung bud mesenchyme and myocardial cells by E9.5, and is activated in developing branchial arches and limb buds by E10.5). Almost all (`95%) of homozygous mice die in utero between E11.5-E12.5 from circulation distress; exhibiting malformed atrial septum, dilated atria with hypoplastic venous valves, and blood backflow from the heart into systemic veins. Homozygotes also exhibit complete agenesis of adrenal glands, metanephric kidneys, gonads, and defects in pericard ..... For more information please see the full phenotype on the strain data sheet | ||
| 002275 | B6.129S4-Ntf3tm1Jae/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Ntf3tm1Jae targeted mutation are smaller than their normal littermates and most die shortly after birth. Survivors die prior to weaning. They display limb ataxia, an inability to position the limbs properly when attempting to move, and there is a tendency for all four limbs to intermittently stiffen in an extensor posture. Autopsy showed all peripheral ganglia markedly smaller in the mutant. Spinal proprioceptive afferents and their peripheral sense organs are completely absent. Heterozygous mice appear normal; however, the number of muscle spindles in heterozygotes is half that of normal wildtype siblings. There is approximately a 50% reduction in the sympathetic superior cervical ganglion (SCG) neurons caused by excessive apoptosis of sympathetic neuroblasts during neurogenesis. | ||
| 003541 | B6.129S4-Ntf3tm2Jae/J | Cryopreserved - Ready for recovery |
| This strain has loxP sites located on either side of the Ntf3 exon 2. Mice homozygous for this allele are viable, fertile and without behavioral abnormalities. If this strain is crossed with a transgenic strain bearing Cre recombinase, expression of the Ntf3 gene in offspring can be blocked in a tissue-specific manner depending on the promoter controlling the recombinase. Strains under the control of the rat nestin promoter block expression in the central nervous system; see strains 002275 and 002276.
When bred to a strain expressing Cre recombinase in skeletal muscle (see Stock No. 007893 for example), this mutant mouse strain may be useful in studies of muscle spindle development | ||
| 006904 | B6;129-Msctm1Eno/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 004234 | B6;129S-Fgfr3tm1Dor/J | Cryopreserved - Ready for recovery |
| Approximately 50% of mice that are homozygous for the Fgfr3tm1Dor targeted mutation die between birth and 21 days of age. Surviving pups may live as long as 8 months. RNAase protection analysis of adult homozygous brain tissue indicates that an abnormal transcript may be generated, but that no functional protein results. Severe skeletal defects (kyphosis, scoliosis, crooked tails, curvature and overgrowth of long bones) are evident. Inner ear defects (lack of pillar cell differentiation and tunnel of Corti formation) resulting in profound deafness are also observed. | ||
| 000221 | B6C3Fe a/a-Alx4lst-J/J | Cryopreserved - Ready for recovery |
| 002522 | C.129S4-Myf5tm1Jae/J | Cryopreserved - Ready for recovery |
| Mice homozygous for a targeted mutation in the Myf5 gene die perinatally from respiratory failure due to improper development of the rib cage. Ribs are truncated and the sternum is shortened, with no sternebral segmentation and no connection to the ribs. Mutant mice show no obvious alterations in the vertebral column in comparison to wild type controls, and there are no skeletal muscle abnormalities apparent at birth. | ||
| 002523 | C.129S4-Myod1tm1Jae/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Histological examination of skeletal muscle reveals no morphological abnormalities. Northern analysis indicates that myogenic factor 5 mRNA levels are elevated in postnatal homozygous mutant mice. This mutant mouse strain may be useful in studies examining the factors involved in differentiation of skeletal muscle. | ||
| 002276 | STOCK Ntf3tm1Jae/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Ntf3tm1Jae targeted mutation are smaller than their normal littermates and most die shortly after birth. Survivors die prior to weaning. They display limb ataxia, an inability to position the limbs properly when attempting to move, and there is a tendency for all four limbs to intermittently stiffen in an extensor posture. Autopsy showed all peripheral ganglia markedly smaller in the mutant. Spinal proprioceptive afferents and their peripheral sense organs are completely absent. Heterozygous mice appear normal; however, the number of muscle spindles in heterozygotes is half that of normal wildtype siblings. There is approximately a 50% reduction in the sympathetic superior cervical ganglion (SCG) neurons caused by excessive apoptosis of sympathetic neuroblasts during neurogenesis. | ||
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