Search Criteria: Research Area is "Developmental Biology Research: Mesodermal Defects (Myogenesis Defects)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 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. | ||
| 002475 | B6.129S1-Myf6tm1Wb/J | Repository-Cryopreserved |
| 002275 | B6.129S4-Ntf3tm1Jae/J | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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. | ||
| 002522 | C.129S4-Myf5tm1Jae/J | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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. | ||
(7 stocks) Back to Top
Send questions to our Technical Support team using the Express Technical Support Form.
(3.2)