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- Description
- Phenotype
- Genes & alleles
- Genotyping
- Health & husbandry
- References
- Purchasing information
- Terms of Use
Description
Strain Information
Former Names FVB.Cg-Tg(SMN2)89Ahmb Smntm1Msd/J (Changed: 10-JAN-05 ) FVB.Cg-Tg(SMN2)89Ahmb Smntm1Msd (Changed: 15-DEC-04 ) Type Congenic; Mutant Strain; Targeted Mutation; Transgenic; Additional information on Genetically Engineered Mutant Mice. Mating System See Colony Maintenance Species laboratory mouse Generation N5F?+9 (01-DEC-08) Donating Investigator Arthur Burghes, The Ohio State University Description
Mice that are homozygous for the targeted mutant Smn1 allele and carry the SMN2 transgene exhibit symptoms and neuropathology similar to patients afflicted with type I proximal spinal muscular atrophy (SMA). In the initial characterization by the donating investigator, mice were either stillborn or survived 4-6 days. Mice that died at or shortly after birth were slightly smaller (1.33 g. vs. 1.51 g.) than normal littermates. Mice that survive for several days are indistinguishable from normal littermates in the first 48 hours, after which they exhibit decreased suckling and movement, labored breathing and tremoring limbs. Mice succumbing at this later time point are noticeably smaller than normal littermates (1.47 g vs. 4.59). A bell-shaped trunk is also noticeable in affected mice, presumably from intercostal muscle weakness, a characteristic of type I SMA. Histological analysis indicates that affected mice that survive to day 5 exhibit a loss of motor neurons from spinal cord (35%) and facial nucleus (40%). A large number of cells with pyknotic nuclei are observed in these tissues. Immunohistochemical analysis indicates low-level expression of the SMN2 protein in the tissues examined (brain, liver, spinal cord) and an absence or near absence of intranuclear aggregates of the SMN protein ('gems'). The donating investigator reports that muscle fibers (quadriceps and gastrocnemius assayed) are atrophied, a characteristic observed in SMA patients. Homozygous mice bearing the Smn1 targeted mutation without a copy of the SMN2 transgene display an embryonic lethal phenotype with developmental arrest occurring prior to implantation.Note: In contrast to the original publication, and possibly due to inbreeding, it is the experience at The Jackson Laboratory that mice hemizygous for the SMN2 transgene do not survive.
Importation of this model was supported by the Spinal Muscular Atrophy Foundation. Creation and development was supported by the National Institutes of Health, the Deutsche Forschungsgemeinschaft to M.S., Families of SMA, the Preston fund, the Madison fund, the Mathew fund and the Muscular Dystrophy Association of America.
Development
The targeted mutant allele was created in the laboratory of Dr. Michael Sendtner at the University of Wurzburg, Germany. Exon 2 of the endogenous mouse Smn1 gene was disrupted by employing a targeting vector encoding a neomycin cassette and a lacZ gene fused to the first 40 nucleotides of the disrupted exon to permit expression of the lacZ gene in tissues where Smn is normally expressed. The construct was electroporated into 129P2/OlaHsd-derived E14Tg2a-IV embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts and chimeric animals obtained. Chimeric animals were crossed to C57BL/6 for an unspecified number of generations. The SMN2 transgene was created in the laboratory of Dr. Arthur Burghes at The Ohio State University. A 35.5 kb BamHI genomic fragment encoding the human SMN2 promoter and gene (derived from genomic clone PAC215P15) was injected into fertilized FVB/N mouse oocytes. Transgenic SMN2 mice from founder line 89 were established and then bred to the Smn1 mutant mice. The double mutant mice were then backcrossed to FVB/N for at least 5 generations.
Control Information
| Control | ||
|---|---|---|
| 001800 FVB/NJ | (approximate) | |
| Appropriate controls depend on the nature of the experiment. FVB/NJ mice (Stock No. 001800) may be used as controls. | ||
| Considerations for Choosing Controls | ||
Related Strains
lacZ Expression Strains
View lacZ Expression Strains (178 strains)
Additional Web Information
Fluorescent Proteins/lacZ Systems
Genetic Quality Control Annual Report
Phenotype
Phenotype Information
Spinal Muscular Atrophy, Type I; SMA1 - Models with phenotypic similarity to human disease where etiologies involve orthologs.1
1 Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
assigned by genotype
Smn1tm1Msd/Smn1tm1Msd Tg(SMN2)89Ahmb/Tg(SMN2)89Ahmb
FVB.Cg-Tg(SMN2)89Ahmb Smn1tm1Msd/J
- nervous system phenotype
- abnormal muscle innervation (MGI Ref ID J:132467)
- mice preferentially lack innervation of the caudal band of the levator auris longus
- abnormal neuromuscular synapse morphology (MGI Ref ID J:132467)
- many endplates are partially occupied or vacant unlike in wild-type mice
- muscle phenotype
- abnormal skeletal muscle fiber morphology (MGI Ref ID J:132467)
- muscle fiber diameter is decreased in both slow- and fast-twitch muscles compared to in wild-type mice
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Smn1tm1Msd/Smn1tm1Msd Tg(SMN2)89Ahmb/0
B6.Cg-Smn1tm1Msd Tg(SMN2)89Ahmb
- lethality-postnatal
- postnatal lethality (MGI Ref ID J:97103)
- mice do not survive past 2 days with a mean survival of 1 day
Smn1tm1Msd/Smn1tm1Msd Tg(SMN2)89Ahmb/?
involves: 129P2/OlaHsd * C57BL/6J * FVB
- lethality-prenatal/perinatal
- perinatal lethality (MGI Ref ID J:60592)
- the majority of mice were stillborn or died within 6 hours of birth
- a slightly less than expected frequency of mice with this genotype suggests that some mice may be dying in utero
- in few cases, mice of this genotype survived up to 6 days of age
- behavior/neurological phenotype
- abnormal suckling behavior (MGI Ref ID J:60592)
- mice that survived 4-6 days displayed a decrease or lack of suckling by 48 hours postnatal
- bradykinesia (MGI Ref ID J:60592)
- mice that survived 4-6 days showed a decrease in movement within 48-72 hours postnatal
- tremors (MGI Ref ID J:60592)
- mice that survived 4-6 days showed a marked tremor within 72-96 hours postnatal
- muscle phenotype
- *normal* muscle phenotype (MGI Ref ID J:60592)
- no musculature atrophy was detected in the quadriceps or gastrocnemius of mice that survived 4-6 days
- respiratory system phenotype
- respiratory distress (MGI Ref ID J:60592)
- mice that survived 4-6 days displayed labored breathing by 48 hours postnatal
- nervous system phenotype
- motor neuron degeneration (MGI Ref ID J:60592)
- dramatic loss of motor neurons were observed in spinal cord (~35% loss) and facial nucleus(~40% loss) at postnatal day 5
- normal numbers of motor neurons were observed in spinal cord and facial nucleus in animals at postnatal day 1
Smn1tm1Msd/Smn1tm1Msd Tg(SMN2)89Ahmb/Tg(SMN2)89Ahmb
B6.Cg-Smn1tm1Msd Tg(SMN2)89AhmbThis mouse can be used to support research in many areas including:
Smn1tm1Msd relatedDevelopmental Biology Research
Neurodevelopmental Defects
Perinatal Lethality
Neurobiology Research
lacZ expression in neural tissue
Ataxia (Movement) Defects
Neurodegeneration
Neurodevelopmental Defects
Neuromuscular Defects
Spinal Muscular Atrophy (SMA)
Research Tools
lacZ Expression
Genetics Research (Tissue/Cell Markers: multiple)
Genetics Research (Tissue/Cell Markers: neurons)
Neurobiology Research (cell marker)
Neurobiology Research
Spinal Muscular Atrophy (SMA)
Genes & Alleles
Gene & Allele Information
| Allele Symbol | Smn1tm1Msd | ||
|---|---|---|---|
| Allele Name | targeted mutation 1, Michael Sendtner | ||
| Allele Type | Targeted (Reporter) | ||
| Common Name(s) | SMN-; | ||
| Mutation Made By | Michael Sendtner, | ||
| Strain of Origin | 129P2/OlaHsd | ||
| ES Cell Line Name | E14Tg2aIV | ||
| ES Cell Line Strain | 129P2/OlaHsd | ||
| Site of Expression | The expression of the lacZ gene in tissues where Smn is normally expressed was noted. | ||
| Gene Symbol and Name | Smn1, survival motor neuron 1 | ||
| Chromosome | 13 | ||
| Gene Common Name(s) | AI849087; BCD541; SMA; SMA1; SMA2; SMA3; SMA4; SMA@; SMN; SMNT; Smn; T-BCD541; expressed sequence AI849087; survival motor neuron; | ||
| Molecular Note | A lacZ-neo cassette was inserted into exon 2 by homologous recombination resulting in an in-frame fusion of lacZ to exon 2. Homozygous mutant embryos were identified up to 80 hours post coitum. The expression of the lacZ gene in tissues where Smn is normally expressed was noted. [MGI Ref ID J:42813] | ||
| Allele Symbol | Tg(SMN2)89Ahmb | ||
| Allele Name | transgene insertion 89, Arthur H M Burghes | ||
| Allele Type | Transgenic (random, expressed) | ||
| Common Name(s) | SMN2; | ||
| Mutation Made By | Arthur Burghes, Ohio State University | ||
| Strain of Origin | FVB/N | ||
| Site of Expression | Dendrites, axons, and soma of spinal motor neurons display distinct expression of GFP. GFP expression mimics endogenous HLXB9 expression pattern. Fluorscence is detected in axons, dendrites, and processes of spinal motor neurons at embryonic day 9.5 to postnatal day 10 aged mice. | ||
| Expressed Gene | SMN2, survival of motor neuron 2, centromeric, human | ||
| Promoter | SMN2, survival of motor neuron 2, centromeric, human | ||
| Molecular Note | A 35.5 kb genomic fragment containing the human survival motor neuron 2 (SMN2) gene and promoter was used for the transgene. The transgene is ubiquitously expressed in all tissues examined by Northern blot analysis. Line 89 carries 1 copy of the transgene. [MGI Ref ID J:60592] | ||
Genotyping
Genotyping Information
Genotyping Protocols
Smn1tm1Msd, MCA, vers. 3
Smn1tm1Msd, STD PCR, vers. 2
Tg(SMN2)89Ahmb, STD PCR, vers. 3
Helpful Links
Optimizing PCR Protocols
References
References
Selected Reference(s)
Monani UR; Sendtner M; Coovert DD; Parsons DW; Andreassi C; Le TT; Jablonka S; Schrank B; Rossol W; Prior TW; Morris GE; Burghes AH. 2000. The human centromeric survival motor neuron gene (SMN2) rescues embryonic lethality in Smn(-/-) mice and results in a mouse with spinal muscular atrophy. Hum Mol Genet 9(3):333-9. [PubMed: 10655541] [MGI Ref ID J:60592]
Additional References
Schrank B; Gotz R; Gunnersen JM; Ure JM; Toyka KV; Smith AG ; Sendtner M. 1997. Inactivation of the survival motor neuron gene, a candidate gene for human spinal muscular atrophy, leads to massive cell death in early mouse embryos. Proc Natl Acad Sci U S A 94(18):9920-5. [PubMed: 9275227] [MGI Ref ID J:42813]
Smn1tm1Msd relatedTg(SMN2)89Ahmb relatedButchbach ME; Edwards JD; Burghes AH. 2007. Abnormal motor phenotype in the SMNDelta7 mouse model of spinal muscular atrophy. Neurobiol Dis 27(2):207-19. [PubMed: 17561409] [MGI Ref ID J:134824]
El-Khodor BF; Edgar N; Chen A; Winberg ML; Joyce C; Brunner D; Suarez-Farinas M; Heyes MP. 2008. Identification of a battery of tests for drug candidate evaluation in the SMNDelta7 neonate model of spinal muscular atrophy. Exp Neurol 212(1):29-43. [PubMed: 18455159] [MGI Ref ID J:137949]
Gavrilina TO; McGovern VL; Workman E; Crawford TO; Gogliotti RG; Didonato CJ; Monani UR; Morris GE; Burghes HM. 2008. Neuronal SMN expression corrects spinal muscular atrophy in severe SMA mice while muscle specific SMN expression has no phenotypic effect. Hum Mol Genet :. [PubMed: 18178576] [MGI Ref ID J:131663]
Jablonka S; Beck M; Lechner BD; Mayer C; Sendtner M. 2007. Defective Ca2+ channel clustering in axon terminals disturbs excitability in motoneurons in spinal muscular atrophy. J Cell Biol 179(1):139-49. [PubMed: 17923533] [MGI Ref ID J:134807]
Jablonka S; Holtmann B; Meister G; Bandilla M; Rossoll W; Fischer U; Sendtner M. 2002. Gene targeting of Gemin2 in mice reveals a correlation between defects in the biogenesis of U snRNPs and motoneuron cell death. Proc Natl Acad Sci U S A 99(15):10126-31. [PubMed: 12091709] [MGI Ref ID J:81784]
Jablonka S; Karle K; Sandner B; Andreassi C; von Au K; Sendtner M. 2006. Distinct and overlapping alterations in motor and sensory neurons in a mouse model of spinal muscular atrophy. Hum Mol Genet 15(3):511-8. [PubMed: 16396995] [MGI Ref ID J:105422]
Jablonka S; Schrank B; Kralewski M; Rossoll W; Sendtner M. 2000. Reduced survival motor neuron (Smn) gene dose in mice leads to motor neuron degeneration: an animal model for spinal muscular atrophy type III. Hum Mol Genet 9(3):341-6. [PubMed: 10655542] [MGI Ref ID J:60591]
Kariya S; Park GH; Maeno-Hikichi Y; Leykekhman O; Lutz C; Arkovitz MS; Landmesser LT; Monani UR. 2008. Reduced SMN protein impairs maturation of the neuromuscular junctions in mouse models of spinal muscular atrophy. Hum Mol Genet 17(16):2552-69. [PubMed: 18492800] [MGI Ref ID J:138437]
Le TT; Pham LT; Butchbach ME; Zhang HL; Monani UR; Coovert DD; Gavrilina TO; Xing L; Bassell GJ; Burghes AH. 2005. SMNDelta7, the major product of the centromeric survival motor neuron (SMN2) gene, extends survival in mice with spinal muscular atrophy and associates with full-length SMN. Hum Mol Genet 14(6):845-57. [PubMed: 15703193] [MGI Ref ID J:97103]
McGovern VL; Gavrilina TO; Beattie CE; Burghes AH. 2008. Embryonic motor axon development in the severe SMA mouse. Hum Mol Genet 17(18):2900-9. [PubMed: 18603534] [MGI Ref ID J:138317]
Monani UR; Pastore MT; Gavrilina TO; Jablonka S; Le TT; Andreassi C; DiCocco JM; Lorson C; Androphy EJ; Sendtner M; Podell M; Burghes AH. 2003. A transgene carrying an A2G missense mutation in the SMN gene modulates phenotypic severity in mice with severe (type I) spinal muscular atrophy. J Cell Biol 160(1):41-52. [PubMed: 12515823] [MGI Ref ID J:81238]
Murray LM; Comley LH; Thomson D; Parkinson N; Talbot K; Gillingwater TH. 2008. Selective vulnerability of motor neurons and dissociation of pre- and post-synaptic pathology at the neuromuscular junction in mouse models of spinal muscular atrophy. Hum Mol Genet 17(7):949-62. [PubMed: 18065780] [MGI Ref ID J:132467]
Novoyatleva T; Heinrich B; Tang Y; Benderska N; Butchbach ME; Lorson CL; Lorson MA; Ben-Dov C; Fehlbaum P; Bracco L; Burghes AH; Bollen M; Stamm S. 2008. Protein phosphatase 1 binds to the RNA recognition motif of several splicing factors and regulates alternative pre-mRNA processing. Hum Mol Genet 17(1):52-70. [PubMed: 17913700] [MGI Ref ID J:130114]
Rose FF Jr; Meehan PW; Coady TH; Garcia VB; Garcia ML; Lorson CL. 2008. The Wallerian degeneration slow (Wld(s)) gene does not attenuate disease in a mouse model of spinal muscular atrophy. Biochem Biophys Res Commun 375(1):119-23. [PubMed: 18680723] [MGI Ref ID J:140130]
Rossoll W; Jablonka S; Andreassi C; Kroning AK; Karle K; Monani UR; Sendtner M. 2003. Smn, the spinal muscular atrophy-determining gene product, modulates axon growth and localization of beta-actin mRNA in growth cones of motoneurons. J Cell Biol 163(4):801-12. [PubMed: 14623865] [MGI Ref ID J:86712]
Schrank B; Gotz R; Gunnersen JM; Ure JM; Toyka KV; Smith AG ; Sendtner M. 1997. Inactivation of the survival motor neuron gene, a candidate gene for human spinal muscular atrophy, leads to massive cell death in early mouse embryos. Proc Natl Acad Sci U S A 94(18):9920-5. [PubMed: 9275227] [MGI Ref ID J:42813]
Walker MP; Rajendra TK; Saieva L; Fuentes JL; Pellizzoni L; Matera AG. 2008. SMN complex localizes to the sarcomeric Z-disc and is a proteolytic target of calpain. Hum Mol Genet 17(21):3399-410. [PubMed: 18689355] [MGI Ref ID J:140332]
Avila AM; Burnett BG; Taye AA; Gabanella F; Knight MA; Hartenstein P; Cizman Z; Di Prospero NA; Pellizzoni L; Fischbeck KH; Sumner CJ. 2007. Trichostatin A increases SMN expression and survival in a mouse model of spinal muscular atrophy. J Clin Invest 117(3):659-71. [PubMed: 17318264] [MGI Ref ID J:120738]
Butchbach ME; Edwards JD; Burghes AH. 2007. Abnormal motor phenotype in the SMNDelta7 mouse model of spinal muscular atrophy. Neurobiol Dis 27(2):207-19. [PubMed: 17561409] [MGI Ref ID J:134824]
Gavrilina TO; McGovern VL; Workman E; Crawford TO; Gogliotti RG; Didonato CJ; Monani UR; Morris GE; Burghes HM. 2008. Neuronal SMN expression corrects spinal muscular atrophy in severe SMA mice while muscle specific SMN expression has no phenotypic effect. Hum Mol Genet :. [PubMed: 18178576] [MGI Ref ID J:131663]
Jablonka S; Beck M; Lechner BD; Mayer C; Sendtner M. 2007. Defective Ca2+ channel clustering in axon terminals disturbs excitability in motoneurons in spinal muscular atrophy. J Cell Biol 179(1):139-49. [PubMed: 17923533] [MGI Ref ID J:134807]
Jablonka S; Karle K; Sandner B; Andreassi C; von Au K; Sendtner M. 2006. Distinct and overlapping alterations in motor and sensory neurons in a mouse model of spinal muscular atrophy. Hum Mol Genet 15(3):511-8. [PubMed: 16396995] [MGI Ref ID J:105422]
Kariya S; Park GH; Maeno-Hikichi Y; Leykekhman O; Lutz C; Arkovitz MS; Landmesser LT; Monani UR. 2008. Reduced SMN protein impairs maturation of the neuromuscular junctions in mouse models of spinal muscular atrophy. Hum Mol Genet 17(16):2552-69. [PubMed: 18492800] [MGI Ref ID J:138437]
Le TT; Pham LT; Butchbach ME; Zhang HL; Monani UR; Coovert DD; Gavrilina TO; Xing L; Bassell GJ; Burghes AH. 2005. SMNDelta7, the major product of the centromeric survival motor neuron (SMN2) gene, extends survival in mice with spinal muscular atrophy and associates with full-length SMN. Hum Mol Genet 14(6):845-57. [PubMed: 15703193] [MGI Ref ID J:97103]
McGovern VL; Gavrilina TO; Beattie CE; Burghes AH. 2008. Embryonic motor axon development in the severe SMA mouse. Hum Mol Genet 17(18):2900-9. [PubMed: 18603534] [MGI Ref ID J:138317]
Monani UR; Pastore MT; Gavrilina TO; Jablonka S; Le TT; Andreassi C; DiCocco JM; Lorson C; Androphy EJ; Sendtner M; Podell M; Burghes AH. 2003. A transgene carrying an A2G missense mutation in the SMN gene modulates phenotypic severity in mice with severe (type I) spinal muscular atrophy. J Cell Biol 160(1):41-52. [PubMed: 12515823] [MGI Ref ID J:81238]
Murray LM; Comley LH; Thomson D; Parkinson N; Talbot K; Gillingwater TH. 2008. Selective vulnerability of motor neurons and dissociation of pre- and post-synaptic pathology at the neuromuscular junction in mouse models of spinal muscular atrophy. Hum Mol Genet 17(7):949-62. [PubMed: 18065780] [MGI Ref ID J:132467]
Novoyatleva T; Heinrich B; Tang Y; Benderska N; Butchbach ME; Lorson CL; Lorson MA; Ben-Dov C; Fehlbaum P; Bracco L; Burghes AH; Bollen M; Stamm S. 2008. Protein phosphatase 1 binds to the RNA recognition motif of several splicing factors and regulates alternative pre-mRNA processing. Hum Mol Genet 17(1):52-70. [PubMed: 17913700] [MGI Ref ID J:130114]
Rossoll W; Jablonka S; Andreassi C; Kroning AK; Karle K; Monani UR; Sendtner M. 2003. Smn, the spinal muscular atrophy-determining gene product, modulates axon growth and localization of beta-actin mRNA in growth cones of motoneurons. J Cell Biol 163(4):801-12. [PubMed: 14623865] [MGI Ref ID J:86712]
Walker MP; Rajendra TK; Saieva L; Fuentes JL; Pellizzoni L; Matera AG. 2008. SMN complex localizes to the sarcomeric Z-disc and is a proteolytic target of calpain. Hum Mol Genet 17(21):3399-410. [PubMed: 18689355] [MGI Ref ID J:140332]
Health & husbandry
Health & Colony Maintenance Information
Animal Health Reports
Room Number AX12
Colony Maintenance
Breeding & Husbandry The Smn1 (survival motor neuron 1) gene on Chr 13 and the randomly inserted transgene are not linked and will segregate independently. Breeding pairs offered by The Jackson Laboratory are homozygous for the transgene and heterozygous for the targeted Smn1 mutation. These breeding pairs are phenotypically normal and do not exhibit symptoms of neuropathology. Offspring resulting from the mating of breeder pairs can posses the following genotypes: 1. Homozygous for the transgene and homozygous for the targeted mutation (25%)
2. Homozygous for the transgene and heterozygous for the targeted mutation (50%)
3. Homozygous for the transgene and wildtype at the Smn1 locus (25%)Mice that are homozygous for the transgene and homozygous for the targeted mutation will display the SMA-like phenotype. Mice homozygous for the transgene and heterozygous for the targeted mutation will not display the SMA-like phenotype but can be mated with each other to generate additional affected mice. Mice homozygous for the transgene and wildtype at the Smn1 locus will also not exhibit an SMA-like phenotype but can be employed as control mice depending on the nature of the experiment. The Jackson Laboratory also distributes mice that are homozygous for the transgene and wildtype at the Smn1 locus.
Note: In contrast to the original publication, and possibly due to inbreeding, it is the experience at The Jackson Laboratory that mice hemizygous for the SMN2 transgene do not survive.
Mating System See above Diet Information LabDiet® 5K52/5K67
Purchasing information
Pricing, Supply Level & Notes, Controls, General Terms & Conditions
Pricing
| Pricing for USA, Canada and Mexico shipping destinations |
|
Weeks of Age Price* Gender Genotypes Provided Individual Mouse Price $229.70 Female or Male Homozygous for Tg(SMN2)89Ahmb, Heterozygous for Smn1tm1Msd $229.70 Female or Male Homozygous for Tg(SMN2)89Ahmb, Wild-type for Smn1tm1Msd *Price(s) in US dollars ($)
Pairs /Price* Pair Genotype $459.40 Homozygous for Tg(SMN2)89Ahmb, Heterozygous for Smn1tm1Msd x Homozygous for Tg(SMN2)89Ahmb, Heterozygous for Smn1tm1Msd
Additional Supply Details
| Supply Notes |
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| Pricing for International shipping destinations |
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Weeks of Age Price* Gender Genotypes Provided Individual Mouse Price $298.70 Female or Male Homozygous for Tg(SMN2)89Ahmb, Heterozygous for Smn1tm1Msd $298.70 Female or Male Homozygous for Tg(SMN2)89Ahmb, Wild-type for Smn1tm1Msd *Price(s) in US dollars ($)
Pairs /Price* Pair Genotype $597.30 Homozygous for Tg(SMN2)89Ahmb, Heterozygous for Smn1tm1Msd x Homozygous for Tg(SMN2)89Ahmb, Heterozygous for Smn1tm1Msd
Additional Supply Details
| Supply Notes |
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Supply Details
| Standard Supply | Repository-Live. A collection of over 1000 strains maintained as live colonies. Individual colonies are sized to meet current customer demand. Delivery for orders of 10 mice or less ranges on average from one to eight weeks; mice are generally shipped between four to six weeks of age with a maximum shipping age of ~nine weeks. Colony sizes do not generally support stringent age specifications for large volumes of mice; however custom orders and larger quantities of mice are easily arranged. Estimated ship dates for all orders provided within 48 hours of order placement. |
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| Supply Notes |
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Control Information
| Control | ||
|---|---|---|
| 001800 FVB/NJ | (approximate) | |
| Appropriate controls depend on the nature of the experiment. FVB/NJ mice (Stock No. 001800) may be used as controls. | ||
| Considerations for Choosing Controls | ||
| USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
| International - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
General Terms and Conditions
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