Search Criteria: Strain Type is "Deletion"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 011128 | B10.SJL-Dysfim/AwaJ | Repository- Live |
| Mice that are homozygous for this mutation exhibit a progressive muscular dystrophy characterized by myofiber degeneration and increased fibrosis. Disease onset on the C57BL/10 background is apparent by 4 weeks of age and is severe by 8 months of age, although, mice can survive until 19 months. During the late stage of the disease muscles exhibit fatty and fibrotic tissue as well as inflammatory cells. Affected muscles include the proximal limbs, (quadriceps femoris and triceps brachii) and abdominals. The distal limbs, (gastocnemius, soleus, and tibialis anterior), diaphram, and biceps brachii appear to be only mildly affected even in the late stages of the disease. Both pyruvate and creatinine kinase levels are increased. Regeneration following notexin-induced muscle damage is impaired by delayed removal of necrotic fibers and an extended inflammatory period. This mutant mouse strain may be useful as a model of limb-girdle muscular dystrophy type 2B (LGMD2B) and Miyoshi myopath ..... For more information please see the full phenotype on the strain data sheet | ||
| 013128 | B6129S-Del(7Slx1b-Sept1)4Aam/J | Repository- Live |
| These mutant mice possess an engineered deletion spanning approximately 0.39 Mb on mouse Chromosome 7. The region involved encompasses a chromosomal segment, between the GIY-YIG domain containing 2 (Giyd2) gene and the septin 1(Sept1) loci, that shares conserved synteny with the Autism spectrum disorders critical interval on human Chromosome 16 (the 16p11.2 region). Mice carrying one copy of the deletion prove to be viable while mice homozygous for the deletion are embryonic lethal. These mice exhibit neuroanatomical and behavioral phenotypes reminiscent of human autism. This mutant mouse may be useful in studying Autism and other associated disorders.
(Mice bearing the reciprocal duplication are also available (see Stock No. 013129)) | ||
| 003374 | B6;129S2-H2dlAb1-Ea/J | Repository- Live |
| Mice that are homozygous null for MHC class II genes H2-Ab1, H2-Aa, H2-Eb1, H2-Eb2, H2-Ea are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. MHC class II gene products (mRNA or protein) are not detected. A dramatic decrease is observed in the number of CD4 positive T cells in thymus, spleen and lymph nodes. This strain should serve as a suitable recipient of xenogenic Class II MHC transgenes allowing the engineering of mouse models of human MHC Class II-associated diseases. | ||
| 012866 | B6N.DDD-plt/NknoJ | Repository- Live |
| Homozygous C57BL/6-plt mice are viable and fertile, harboring the spontaneous plt (or "paucity of lymph node T cells") deletion of both the Ccl19 and Ccl21a loci on chromosome 4. Lack of expression of these two CCR7 ligands in the secondary lymphoid organs results in abnormal leukocyte migration and impaired immune response. Specifically, homozygous mice have disrupted trafficking/homing of T cells and dendritic cells to lymphoid tissues. No reported abnormalities in B cell distribution/cellularity are reported for homozygous mice. Transient migration of antigen-stimulated B cells in lymphoid organs (which facilitates B cell/helper T cell interactions) is also impaired in homozygous mice. Homozygous mice exhibit mature single-positive thymocyte arrest in the thymic cortex that results in defective formation of the medullary region of the thymus. Thymic export of T cells in these mice is compromised during the neonatal period but not in adulthood. While C ..... For more information please see the full phenotype on the strain data sheet | ||
| 002802 | C3.BLiA Pde6b+-Krd/J | Repository- Live |
| This is a semidominant, homozygous lethal mutation. | ||
| 006653 | 129S-Del(6)1Mom/MomJ | Cryopreserved - Ready for recovery |
| Using chromosome engineering technology, an approximately 600 kilobase genomic region was deleted that contains a cluster of 16 intact V1r vomeronasal receptor genes. The mutant mice display deficits in a subset of VNO-dependent behaviors: the expression of male sexual behavior and maternal aggression is substantially altered. Electrophysiologically, the epithelium of the VNO of such mice does not respond detectably to specific pheromonal ligands. | ||
| 005730 | 129S6.CB(B6)-Del(1)1Brk Gpi1b/Gpi1c/BrkMdfJ | Cryopreserved - Ready for recovery |
| Homozygous mice develop microcytic anemia, sparse hair, enlarged spleens and a slight cardiomegaly. Males are infertile. Homozygous mice on the C57BL/6J background develop hydrocephalus and less than 5% survive beyond 6 days. On the 129 background, 95% of mice survive to adulthood. | ||
| 005535 | B6.129S7-Del(11Cops3-Rnf112)1Jrl/J | Cryopreserved - Ready for recovery |
| 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 phenotype on the strain data sheet | ||
| 002283 | B6.Cg-KitW-19H/EiJ | Cryopreserved - Ready for recovery |
| This deletion is a dominant mutation causing white spotting on the feet, tail, belly, and occasionally elsewhere. Homozygosity is embryonic lethal. On the C57BL/6 background approximately 60% of heterozygous females have a closed vagina. The ovaries from these heterozygotes are normal and fine for transplantation. On the C57BL/6 background in the presence of the YAKR/J Chromosome (available from Stock No. 007250), KitW-19H heterozygosity results in sex reversed XY females. | ||
| 006790 | B6;129P2-Del(14)3Mom/MomJ | Cryopreserved - Ready for recovery |
| The H element was identified by the high homoology of this non-coding DNA between mouse and human. In hemizygotes, the Del(14)3Mom deletion of the H element abolishes expression of Olfr1507 (MOR28) and Olfr1508 (MOR10) genes in cis from the 129P2/OlaHsd chromosome, while expression of Olfr1507 and Olfr1508 genes from the wild-type C57BL/6J chromosome persists. In homozygotes, Olfr1507, Olfr1508, and Olfr1509 (MOR83) genes are not expressed, and there is a graded, distance-related decrease in the numbers of cells expressing more distal olfactory receptor genes, Olfr1510 (MOR29A), Olfr1511 (MOR29B), Olfr1512 (MOR30A), and Olfr1513 (MOR30B). The expression of other olfactory receptor genes on Chromosome 14 such as Olfr1514 (MOR205-1), Olfr749 ((S1), and Olfr221 (MOR205-1) is not affected in an obvious way by the Del(14)3Mom deletion. Expression of olfactory receptor genes locate ..... For more information please see the full phenotype on the strain data sheet | ||
| 005654 | B6C3-Del(16Cbr1-ORF9)1Rhr/J | Cryopreserved - Ready for recovery |
| These mice are monosomic for the mouse chromosome segment MMU16. The deleted segment contains mouse orthologs of 33 conserved and minimally conserved genes in the human Down's syndrome critical region (DSCR). The borders of the deletion are defined by the carbonyl reductase 1 (Cbr1) gene and a site adjacent to the myxovirus (influenza virus) resistance 2 (Mx2) locus. Monosomic mice are viable, fertile and are significantly smaller than wildtype (euploid) littermates from birth to adulthood. This mouse may be useful in studies of Down syndrome and further exploring the ploidy of DSCR/MMU16. | ||
| 008044 | B6C3Fe a/a-bpck/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the bpck deletion develop bilateral polycystic kidneys and die by 3 weeks of age. There is an increased incidence of hydrocephalus. Homozygotes can be identified by their smaller size and swollen abdomens. At 2 weeks of age elevated blood urea nitrogen is found. Ovaries and testes are smaller than normal and progression of maturing cells from spermatocytes to spermatids is disorganized at 3 weeks of age. The primary cilia on the kidney proximal tubule epithelial cells are dysmorphic and vary in length at birth and by 14 days of age cilia are significantly longer than normal. Through overlapping BAC rescues the polycystic kidney disease and hydrocephalus has been traced to the absence of the Tmem67 gene. Although lacking some of the ancillary phenotypes associated with Meckel Syndrome Type 3 in humans, this deletion offers a model for that disease. | ||
| 006549 | B6C3Fe-Del(2Hoxd8,Hoxd9-Hoxd13)1Cx/Cx | Cryopreserved - Ready for recovery |
| Heterozygous mice exhibit a visible hindlimb paralysis. A much more severe paralysis with digit abnormalities is observed in homozygous mice. | ||
| 004406 | C3HeB/FeJ-Pou3f4del-J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Pou3f4del-J display head shaking and circling behavior by three weeks of age. Homozygous females and males hemizygous for this X-linked mutation have profound deafness, although heterozygous females do not. They have cochlear hypoplasia, a reduced number of cochlear turns, failure to fully form the bony structure of the modiolus, and detachment of the stria vascularis. | ||
| 002142 | STOCK 11R30m/J | Cryopreserved - Ready for recovery |
| 004711 | STOCK Ednrbs-52Pub | Cryopreserved - Ready for recovery |
| 013129 | B6129S-Dp(7Slx1b-Sept1)5Aam/J | Under Development - Now Accepting Orders |
| These mutant mice possess an engineered duplication of approximately 0.39 Mb of mouse Chromosome 7. The region involved encompasses a chromosomal segment, between the GIY-YIG domain containing 2 (Giyd2) gene and the septin 1(Sept1) loci, that shares conserved synteny with Autism spectrum disorders (ASD) critical interval on human Chromosome 16, specifically the 16p11.2 region. Homozygous mutant mice are viable and fertile. These mice exhibit neuroanatomical and behavioral phenotypes. This mutant mouse may be useful in studying Autism and other associated disorders.
(Mice bearing the reciprocal deficiency mutation are also available (see Stock No. 013128) | ||
| 017359 | B6;129S2-Cxadrtm1.1Ics/J | Under Development - Now Accepting Orders |
| These mice possess loxP sites on either side of exon 2 of the coxsackie virus and adenovirus receptor gene (Cxadr), a cell adhesion molecule critical in early embryogenesis. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 2 deleted in the cre-expressing tissues.
When bred to a strain with widespread cre/Esr1 expression (Stock No. 00 4682), this mutant mouse strain may be useful in studies of cardiac, gastrointestinal, pancreatic, and thymic development and physiology. | ||
| 012873 | C.DDD-plt/NknoJ | Under Development - Now Accepting Orders |
| Homozygous BALB/c-plt mice are viable and fertile, harboring the spontaneous plt (or "paucity of lymph node T cells") deletion of both the Ccl19 and Ccl21a loci on chromosome 4. Lack of expression of these two CCR7 receptor ligands in the secondary lymphoid organs results in abnormal leukocyte migration and impaired immune response. Specifically, homozygous mice have disrupted trafficking/homing of T cells and dendritic cells to lymphoid tissues. No reported abnormalities in B cell distribution/cellularity are reported for homozygous mice. Homozygous mice exhibit mature single-positive thymocyte arrest in the thymic cortex that results in defective formation of the medullary region of the thymus. Thymic export of T cells in these mice is compromised during the neonatal period but not in adulthood. While CCL21 expression is absent in lymphoid organs because of the Ccl21a deletion, CCL21 expression in non-lymphoid organs is observed because the upstre ..... For more information please see the full phenotype on the strain data sheet | ||
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