Search Criteria: Research Area is "Developmental Biology Research: Embryonic Lethality (Homozygous) (incomplete)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 008001 | 129S-Dvl2tm1Awb/J | Repository- Live |
| Half of homozygotes exhibit a perinatal lethal phenotype. Surviving homozygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Some newborn homozygotes fail to survive and exhibit breathing difficulties, cyanosis and reduced mobility. No gene product (protein) is detected by Western blot analysis of brain lystates. Some nonviable homozygotes display cardiac abnormalities. Most homozygotes (90%) have mild abnormalities of the ribs and vertebrae. 2 to 3% of the homozygous embryos display thoracic spina bifida and exencephaly. This mutant mouse strain may be useful in studies of bone and cardiac development, neural tube closure and spina bifida. | ||
| 007205 | 129S-Myo1eGt(ROSA)74Sor/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). Homozygotes occur at lower than Mendelian ratio (15%). Although homozygotes are fertile, pregnancy is occasionally lethal for homozygous females. Heterozygotes are viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. These Myo1e-mutant mice may be useful in studying vascular development, hematopoiesis and cellular signaling during development and in 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. | ||
| 006141 | B6.129S2-Thbs1tm1Hyn/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile, with an approximate 20% decrease in embryo/neonate viability and a mild and variable lordotic curvature of the spine apparent from birth. Homozygous mice have an abnormal, but no full length transcript in multiple tissues. Western analysis confirmed the absence of the protein in platelets. Homozygotes exhibit an increase in the number of circulating white blood cells. During the first four to ten weeks of life, homozygotes exhibit patches of acute and organizing pneumonia. At later time points, there is considerable hyperplasia of the various epithelial cell lineages. Mutant mice also have an increased number of retinal endothelial cells and inappropriate remodeling and maturation of retinal vasculature following injury. On the FVB/N background, spontaneous tumor growth and vasculature are significantly increased compared to wildtype. Mutant mice may be useful in studies of inflammatory responses in the lungs, eye, and
..... 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 | ||
| 004669 | B6;129S2-Itgb3tm1Hyn/J | Repository- Live |
| Mice that are homozygous for this targeted allele are viable and fertile. No gene product (protein) is detected on the surface of platelets. Significant (50%) embryonic lethality attributed to fetal hemorrhaging and placental defects is observed. Until three weeks of age, additional pup loss may occur due to hemorrhaging in the skin and gastrointestinal tract. Gastrointestinal tract bleeding is commonly observed in adults and is frequently associated with an enlarged spleen. Erythrocyte number, hemoglobin, hematocrits and thrombus formation are all reduced while bleeding time is prolonged. Varying degrees of liver and kidney necrosis are also observed. Although increased numbers of osteoclasts are observed (3.5 fold over that seen in heterozygotes) they appear to be dysfunctional, having a reduced ability to resorb whale dentin in vitro. Mice are osteosclerotic and hypocalcemic. Enhanced tumor angiogenesis and vascular endothelial growth factor-induced blood vessel growth are observed.
..... For more information please see the full descriiption on the strain data sheet | ||
| 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 | ||
| 005987 | 129-Achetm1Loc/J | Repository-Cryopreserved |
| Homozygous mice have 25% fetal mortality. Those born have retarded growth, fine motor tremors, unusual posture and gait, no righting reflex, malformed pinna, and sealed eyelids. These mice die emaciated and dehydrated by 3 weeks of age. Enriched diets for the nursing female and pups allow homozygous mice to survive to adulthood. Males exhibit no breeding behavior. Homozygous females can become pregnant when bred to heterozygous or wildtype males, but both female and pups do not survive. Acetylcholinesterase (AChE) activity is completely abrogated in serum and tissue from homozygous mice, and approximately half in heterozygotes. Many symptoms of organophosphate poisoning are observed in homozygous mice, including pulsating paws, body tremor, abnormal gait, pinpoint pupils, muscle weakness, and early death following seizure. When restrained, a white mucus forms on the eyes and seizures may occur. Mice also have several developmental delays, low body mass, decreased pain response, sexual
..... For more information please see the full descriiption on the strain data sheet | ||
| 004290 | 129-Ihhtm1Amc/J | Repository-Cryopreserved |
| Mice that are heterozygous for the targeted allele are viable and fertile. Mice homozygous for this mutation have a lethal phenotype. Half of homozygous null mice have an embryonic lethal phenotype, dying between 10.5 to 12.5 days post coitum. The cause of embryonic death may be due to circulatory abnormalities. Embryonic death also occurred in late gestation, with the remaining homozygous mutants dying at birth, due to respiratory failure. At 12.5 dpc, initial cartilaginous primordia of mutant embryos forelimbs are not abnormal, but by 13.5 dpc, mutant embryos display severe foreshortening of the forelimbs. At birth, the length of long bones of mutant animals are only one third the length of long bones of wildtype animals. Mutants have reduced chondrocyte proliferation, abnormal chondrocyte maturation and absence of mature osteoblasts in endochondral bones. Recent studies have linked mutations of Ihh to brachydactyly type A-1 St-Jacques. This mutant mouse strain represents a mo
..... For more information please see the full descriiption on the strain data sheet | ||
| 004445 | B6.129S2-Creb1tm1Gsc/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. In heterozygote crosses, the number of homozygous progeny born (15%) does not reach the expected Mendelian ratio indicating low survival of homozygous embryos. No gene product (mRNA or alpha and delta isoform proteins) is detected. The beta isoform gene product is up regulated. cAMP response element modulation protein expression is up regulated 2- to 3-fold. Although fear conditioning and Morris water maze testing demonstrate that homozygous mice have normal learning and short-term memory, long-term memory for cued and contextual conditioning is disrupted. Electrophysiological analysis of the hippocampus of mutant mice reveals abnormal long-term potentiation, which decays to baseline within 90 minutes, whereas wildtype controls display no decay. The long-term memory deficit exhibited by mutant mice can be overcome by additional spaced (10-60 m
..... For more information please see the full descriiption on the strain data sheet | ||
| 004078 | B6.129S2-F5tm1Dgi/J | Repository-Cryopreserved |
| Approximately half of the mice that are homozygous null for the F5 gene die at embryonic day 9-10. Those that develop beyond this stage continue to develop but suffer from massive intra-abdominal hemorrhages and die within two hours of birth. Also observed are microscopic hemorrhages in a variety of tissues. Blood present in the intra-abdominal cavity is unclotted and completely deficient of factor V activity. | ||
| 003865 | B6.129S2-Itgavtm1Hyn/J | Repository-Cryopreserved |
| The majority (80%) of homozygous null Itgav mice die during embryonic days 9.5-11.5. These mice are characterized by pericardial edema and retarded growth probably due to placental defects. Mice surviving this period die at birth exhibiting intracranial and intestinal hemorrhaging. Angiogenesis in other tissues is normal. Cleft palate is also observed. | ||
| 002862 | B6.129S4-F2rtm1Ajc/J | Repository-Cryopreserved |
| About half of the homozygous mice die at around embryonic day 9-10. The surviving homozygotes are fertile. Platelets from surviving homozygotes respond to thrombin while fibroblasts from the same mice are unable to respond to thrombin. | ||
| 004425 | B6;129-Gdf1tm1Sjl/J | Repository-Cryopreserved |
| Mice that are heterozygous for the targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous null mice have an embryonic and perinatal lethal phenotype, most develop past embryonic day 14.5 with two thirds dying at birth and almost all not surviving beyond 48 hours after birth. Homozygous mutant newborn mice display a range of left-right axis defects such as visceral situs inversus, right pulmonary isomerism and cardiac anomalies including abnormal positioning of the aorta and pulmonary artery, and septal defects. Spleen and lungs were malformed in some homozygotes. This mutant mouse strain represents a model that may be useful in studies of situs inversus. | ||
| 004995 | C3H-Tg(Camk2a-Creb1/ESR1)3Sva/J | Repository-Cryopreserved |
| These transgenic mice have a tamoxifen inducible cAMP responsive element binding protein 1 (Creb1) repressor driven by the mouse calcium/calmodulin-dependent protein kinase II alpha promoter. The transgene insert contains a fusion product involving a mutant Creb1 isoform (CREBS133A) and a mutant form of the human estrogen receptor ligand binding domain (LBDG521R). Expression of the transgene is detected in the hippocampus and cortex as analyzed by Northern and Western blot. In addition, transgene expression is detected in the amygdala by RT-PCR analysis. The mutant human estrogen receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen. Tamoxifen administration activates the repressor, reducing cyclic AMP responsive element-mediated transcription. When the repressor system is activated, mutant mice exhibit impaired long term memory consolidation and retrieval in fear conditioning tra
..... For more information please see the full descriiption on the strain data sheet | ||
| 001595 | DW/J-Acdacd/J | Repository-Cryopreserved |
| acd/acd homozygotes can be distinguished from their wildtype (?/+) littermates by darkened pigmentation, short, curly vibrissae, smaller overall size, and abnormal pelage. Hair growth is retarded and lacks zigzag and guard hairs producing a sparse coat. There is heavy pigmentation in the nose, ears, body, feet and tail, and foci of melanin are also found in the skin and lymph nodes. Tail kinks or polydactyly of the hind feet are sometimes found and external genitalia are underdeveloped. It is rare for homozygotes to breed. Hydronephrosis is sometimes found in post-wean aged homozygotes resulting from focal hypertrophy of ureteral epithelium which causes ureteral blockage. The adrenals are abnormal in both males and females. Although the size of the medullary cells is normal, the cortical cells and nuclei are much larger than normal with nuclear inclusions and many mitochondria in the cytoplasm. These mitochondria have tubular cristae and cholesterol ester droplets, whic
..... For more information please see the full descriiption on the strain data sheet | ||
| 000264 | SM/Ckc-Fbxw4Dac/J | Repository-Cryopreserved |
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