Overview

Also Known As:SMN2;SMN^RT;Smn-

The SMN2;SMN^RT;Smn- triple mutant mouse expresses a modified SMNdelta7 cDNA with a single nucleotide change that allows read-through of the exon 8 stop codon; resulting in increased stability and a modestly more functional SMN protein. These SMN2;SMN^RT;Smn- mice are an intermediate SMN2-based model for studying proximal spinal muscular atrophy (SMA); having a longer lifespan than the SMNdelta7 model (Stock No. 005025), but with a phenotype severe enough for relatively rapid analysis of therapeutics.

Donating Investigator

Christian L Lorson, University of Missouri

Genetic overview

Genetic Background	Generation

Grm7^{Tg(SMN2)89Ahmb}

Allele Type
Transgenic (Hypomorph, Inserted expressed sequence, Humanized sequence)

Smn1^tm1Msd

Allele Type	Gene Symbol	Gene Name
Targeted (Reporter, Null/Knockout)	Smn1	survival motor neuron 1

Tg(SMN1-SMN2*)16Cll

Allele Type
Transgenic (Inserted expressed sequence, Humanized sequence)

View Genetics

Research Applications

Research Tools
Neurobiology Research
Developmental Biology Research

View All Research Applications

Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

The SMN2;SMN^RT;Smn- triple mutant mouse harbors two transgenes and a single targeted mutation. The Tg(SMN2)89Ahmb transgene (SMN2) expresses the entire human SMN2 gene, whereas no endogenous Smn1 expression is observed from the Smn1 null targeted mutation (Smn1^tm1Msd; also called Smn1^-). The SMN read-through transgene (SMN^RT) has an identical SMN cDNA as the SMNdelta7 cDNA except that a single nucleotide change in exon 8 converts the SMNdelta7 stop codon to tyrosine, allowing read-through and addition of four more amino acids to the expressed SMN protein; resulting in increased stability and a modestly more functional SMN protein.
Regarding expression levels, SMN protein levels in hemizygous SMN^RT transgenic line 16 mice are similar to hemizygous SMNdelta7 mice in brain, spinal cord and skeletal muscle, and the SMN protein levels in both animals are significantly reduced compared to unaffected animals. The SMN^RT transgene in line 16 has a Mendelian inheritance pattern indicative of a single integration event. The donating investigator also reports the transgene copy number was stable via qPCR.

Mice that are homozygous for the Tg(SMN2)89 transgene, hemizygous for the SMN^RT transgene, and homozygous for the Smn1 null mutation (SMN2+/+;SMN^RT;Smn-/-) have mean lifespan of 34 days and begin showing signs of necrosis on the ears, tail and/or eye at approximately 40-50 days of age. Nearly 25% of the SMN2+/+;SMN^RT;Smn-/- animals live beyond 40 days, with several animals living beyond 70 days. Mice that are homozygous for both transgenes and homozygous for the Smn1 null mutation (SMN2+/+;SMN^RT/RT;Smn-/-) also exhibit mild necrosis and have similar lifespan.

Compared to the moderate type II SMA mouse model of similar genotype (SMN2+/+;SMNdelta7+/-;Smn-/- mice; Stock No. 005025), these SMN2+/+;SMN^RT;Smn-/- mice have extended lifespan, increased weight gain, enhanced strength and physical capabilities, significant improvement in skeletal muscle, intermediate NMJ pathology, and milder cardiac pathology. More specifically, the mean lifespan of SMN2+/+;SMN^RT;Smn-/- is 34 days; significantly longer than the severe type I SMA mouse model (SMN2+/+;Smn-/- mice; Stock No. 005024) (7 days) and the moderate type II SMA mouse model (SMN2+/+;SMNdelta7+/-;Smn-/- mice; Stock No. 005025) (13 days).

Development

These SMN2;SMN^RT;Smn- mice harbor several mutations/transgenes, as described below.

The creation of the Tg(SMN2)89 transgene (SMN2) and Smn1 null targeted mutation (Smn1^tm1Msd; also called Smn1^-) are described for the severe type I SMA mouse model on an FVB/NJ background; Stock No. 005024. Note the Tg(SMN2)89 transgene insertion site is on chromosome 6. These mice were bred to and maintained upon an FVB/NJ background prior to being used for breeding as below.

The SMN^RT transgene was designed by Dr. Christian L. Lorson (University of Missouri) with a 3.4 kbp promoter sequence from the human SMN1 gene, 5' UTR from the human SMN1 gene, a CDNA sequence encoding the SMN read-through protein (SMN^RT; see details below), and the 3' UTR from the human SMN1 gene. To create the SMN^RT CDNA sequence, the complete coding sequence of SMNdelta7 was obtained from Dr. Arthur H.M. Burghes (The Ohio State University Medical Center; see 005025). The SMNdelta7 cDNA sequence, already containing the silent C-to-T transition in exon 7 that results in the alternatively spliced transcript without exon 7, was further modified by Dr. Lorson to change the first stop codon in exon 8 from TAG (STOP) to TAT (tyrosine). After the tyrosine, four additional amino acids (serine, serine, threonine and lysine) are incorporated prior to recognizing the next stop codon. The resulting SMN cDNA sequence, modified to encode a modestly more functional protein, is referred to as SMN read-through (SMN^RT). The complete 5.2 kbp SMN^RT transgene was microinjected into the pronucleus of FVB/N embryos. Transgenic founder animals were bred to non-transgenic cohorts to establish the colony. Mice from founder line 16 had SMN protein expression levels most comparable with SMNdelta7 levels in disease relevant tissues, as well as a Mendelian inheritance pattern indicative of a single integration event. SMN^RT founder male 16 was bred to FVB.SMN2;Smn- females (Stock No. 005024) to generate the SMN2;SMN^RT;Smn- colony.

In 2014, SMN2;SMN^RT;Smn- animals with white coat color on a predominantly FVB genetic background (some C57BL/6 and 129 contributions from the FVB.SMN2;Smn- breeding) were sent to The Jackson Laboratory Repository as Stock No. 018916. Upon arrival, male mice were bred to non-affected females from the severe type I SMA strain (Stock No. 005024; hemizygous for the Tg(SMN2)89 transgene and wildtype at the Smn1 locus) to establish our live colony. Thereafter, this SMN2;SMN^RT;Smn- triple mutant strain was maintained by breeding mice homozygous for the two transgenes and either heterozygous for Smn1^tm1Msd or wildtype at the Smn1 locus.

Expression Data

Expressed Gene	SMN2, survival of motor neuron 2, centromeric, human
Site of Expression	Grm7^{Tg(SMN2)89Ahmb}
Expressed Gene	lacZ, beta-galactosidase, E. coli
Site of Expression	The expression of the lacZ gene in tissues where Smn is normally expressed was noted.
Expressed Gene	SMN2, survival of motor neuron 2, centromeric, human
Site of Expression	Reduced levels of SMN protein are expressed in brain, spinal cord, and skeletal muscle.

Control Suggestions

Wild-type from the colony

Additional Information

Considerations for Choosing Controls

Selected References

Cobb MS; Rose FF; Rindt H; Glascock JJ; Shababi M; Miller MR; Osman EY; Yen PF; Garcia ML; Martin BR; Wetz MJ; Mazzasette C; Feng Z; Ko CP; Lorson CL. 2013. Development and characterization of an SMN2-based intermediate mouse model of Spinal Muscular Atrophy. Hum Mol Genet 22(9):1843-55PubMed: 23390132 MGI: J:194969

View All References

Genetics

Grm7^{Tg(SMN2)89Ahmb}

Allele Symbol: Grm7^{Tg(SMN2)89Ahmb}

Allele Name	transgene insertion 89, Arthur H M Burghes
Allele Type	Transgenic (Hypomorph, Inserted expressed sequence, Humanized sequence)
Allele Synonym(s)	SMN2
Gene Symbol and Name	Grm7, glutamate receptor, metabotropic 7
Gene Synonym(s)
Promoter	SMN2, survival of motor neuron 2, centromeric, human
Expressed Gene	SMN2, survival of motor neuron 2, centromeric, human
Site of Expression	Grm7^{Tg(SMN2)89Ahmb}
Strain of Origin	FVB/N
Chromosome	6
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 integrated into intron 4 of the gene. RT-PCR confirmed reduced expression of the gene the transgene is integrated into.
Mutations Made By	Arthur Burghes, The Ohio State University

Smn1^tm1Msd

Allele Symbol: Smn1^tm1Msd

Allele Name	targeted mutation 1, Michael Sendtner
Allele Type	Targeted (Reporter, Null/Knockout)
Allele Synonym(s)	SMN^-
Gene Symbol and Name	Smn1, survival motor neuron 1
Gene Synonym(s)
Expressed Gene	lacZ, beta-galactosidase, E. coli
Site of Expression	The expression of the lacZ gene in tissues where Smn is normally expressed was noted.
Strain of Origin	129P2/OlaHsd
Chromosome	13
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.
Mutations Made By	Michael Sendtner

Tg(SMN1-SMN2*)16Cll

Allele Symbol: Tg(SMN1-SMN2*)16Cll

Allele Name	transgene insertion 16, Christian L Lorson
Allele Type	Transgenic (Inserted expressed sequence, Humanized sequence)
Allele Synonym(s)	SMN^RT
Gene Symbol and Name	Tg(SMN1-SMN2*)16Cll, transgene insertion 16, Christian L Lorson
Gene Synonym(s)
Promoter	SMN1, survival of motor neuron 1, telomeric, human
Expressed Gene	SMN2, survival of motor neuron 2, centromeric, human
Site of Expression	Reduced levels of SMN protein are expressed in brain, spinal cord, and skeletal muscle.
Strain of Origin	FVB/N
Chromosome	UN
Molecular Note	This transgene consists of 3.4 kb promoter and 5'-untranslated region from the human SMN1 gene, the complete coding sequence of human SMN2 cDNA containing the silent C to T transition in exon 7 that results in the alternatively spliced transcript without exon 7 (SMNdelta7) and a TAG to TAT alteration in the first stop codon in exon 8 (change from a stop codon to a tyrosine), and the 3'-UTR of SMN1. The TAG to TAT change in exon 8 allows for translational stop codon read-through of the SMNdelta7 and generates an extended SMN2 protein. Thirteen lines were produced.

Disease/Phenotype

Disease Terms

Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.

Werdnig-Hoffmann disease

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Research Tools
- lacZ Expression
- Neurobiology Research
Neurobiology Research
- Ataxia (Movement) Defects
- Neurodevelopmental Defects
- Neuromuscular defects
- Spinal Muscular Atrophy (SMA)
- Neurodegeneration
- lacZ expression in neural tissue
Developmental Biology Research
- Neurodevelopmental Defects

Genotype: Smn1^tm1Msd related

Neurobiology Research
- Spinal Muscular Atrophy (SMA)

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Smn1^tm1Msd/Smn1^tm1Msd Tg(SMN1-SMN2)16Cll/0 Grm7^{Tg(SMN2)89Ahmb}/Grm7^{Tg(SMN2)89Ahmb}
involves: 129P2/OlaHsd C57BL/6 * FVB/N

behavior/neurological phenotype

decreased grip strength
- mutants show a slight decrease in grip strength compared to unaffected controls (mice homozygous for Tg(SMN2)89Ahmb and heterozygous for Smn1^tm1Msd)

impaired coordination
- mutants stay on the rotorod for shorter periods of time than unaffected controls (mice homozygous for Tg(SMN2)89Ahmb and heterozygous for Smn1^tm1Msd)

impaired righting response
- 20-70% of mutants at P5-15 are able to right themselves compared to 100% of unaffected control mice (mice homozygous for Tg(SMN2)89Ahmb and heterozygous for Smn1^tm1Msd)
- starting at P5, mutants show increased ability to right compared to triple transgenics homozygous for Smn1^tm1Msd and Tg(SMN2)89Ahmb and hemizygous for Tg(SMN2*delta7)4299Ahmb (20-70% vs. 3-15% in the controls)

growth/size/body region phenotype

decreased body size
- smaller size compared to wild-type controls at P12, although weight is greater than in double homozygous Smn1^tm1Msd and Tg(SMN2)89Ahmb control mice and some mutants eventually reach the weight of unaffected mice

integument phenotype

epidermal necrosis
- mutants start to show signs of necrosis on the ears, tails, and/or eyes at approximately P40-P50

mammalian phenotype

behavior/neurological phenotype
- Normal - mutants are more agile and generally fitter than double homozygous Smn1^tm1Msd and Tg(SMN2)89Ahmb control mice

mortality/aging

premature death
- mean lifespan is 34 days, with mutants living longer than double homozygous Smn1^tm1Msd and Tg(SMN2)89Ahmb control mice
- nearly 25% of mutants live beyond 40 days, with several living beyond P70

muscle phenotype

decreased skeletal muscle fiber size
- skeletal muscle fibers are smaller than in wild-type controls, however they are larger than in triple transgenics homozygous for Smn1^tm1Msd and Tg(SMN2)89Ahmb and hemizygous for Tg(SMN2*delta7)4299Ahmb

nervous system phenotype

abnormal neuromuscular synapse morphology
- mutants exhibit a modest but significant reduction in neuromuscular junction innervation in the longissimus muscle
- mutants show an approximate 60% reduction of proprioceptive synapses onto motor neurons compared to triple transgenics homozygous for Smn1^tm1Msd and Tg(SMN2)89Ahmb and hemizygous for Tg(SMN2*delta7)4299Ahmb
- P19 mutants show an increase in the percentage of neuromuscular junctions with perforated or fragmented endplates compared to controls homozygous for Tg(SMN2)89Ahmb, indicating a defect in synapse maturation

cardiovascular system phenotype

cardiac interstitial fibrosis
- interstitial fibrosis is significantly improved when compared to triple transgenic controls homozygous for Smn1^tm1Msd and Tg(SMN2)89Ahmb and hemizygous for Tg(SMN2*delta7)4299Ahmb
- mutants exhibit a modest, but significant increase in cardiac interstitial fibrosis compared to unaffected wild-type controls

thin interventricular septum
- mutants show a slight reduction in interventricular septum thickness, although this does not reach significance
- the interventricular septum thickness is significantly improved compared to triple transgenic controls homozygous for Smn1^tm1Msd and Tg(SMN2)89Ahmb and hemizygous for Tg(SMN2*delta7)4299Ahmb

cellular phenotype

epidermal necrosis
- mutants start to show signs of necrosis on the ears, tails, and/or eyes at approximately P40-P50

References

Cobb MS; Rose FF; Rindt H; Glascock JJ; Shababi M; Miller MR; Osman EY; Yen PF; Garcia ML; Martin BR; Wetz MJ; Mazzasette C; Feng Z; Ko CP; Lorson CL. 2013. Development and characterization of an SMN2-based intermediate mouse model of Spinal Muscular Atrophy. Hum Mol Genet 22(9):1843-55PubMed: 23390132 MGI: J:194969

Additional - Grm7^{Tg(SMN2)89Ahmb} related

Additional - Smn1^tm1Msd related

Additional - Tg(SMN1-SMN2*)16Cll related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Smn1
- Sanger sequencing:Tg(SMN1-SMN2*)16Cll
- Standard PCR:Grm7 Alternate1
- QPCR:Tg(SMN2*)
- Probe:Grm7-Probe
- Genotyping resources and troubleshooting
Breeding Considerations

The Tg(SMN2)89 transgene on chromosome 6, the Smn1 null targeted mutation (Smn1^tm1Msd) on chromosome 13, and the randomly inserted SMN^RT transgene (Tg(SMN1-SMN2*)16Cll) are not linked and will segregate independently. Breeding pairs offered by The Jackson Laboratory Repository are homozygous for the two transgenes and heterozygous for Smn1^tm1Msd. 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 both transgenes and homozygous for the targeted mutation (25%)
2. Homozygous for both transgenes and heterozygous for the targeted mutation (50%)
3. Homozygous for both transgenes and wildtype at the Smn1 locus (25%)
Mice that are homozygous for both transgenes and homozygous for the targeted mutation will display the SMA-like phenotype. Mice homozygous for both transgenes 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 both transgenes 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.
- Additional Breeding and Husbandry Support
Citation
When using the SMN2;SMN^RT;Smn- mouse strain in a publication, please cite the originating article(s) and include JAX stock #018916 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Pricing & Availability

Cryo Recovery

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
	Homozygous for Tg(SMN2)89Ahmb ,Heterozygous or Wildtype for Smn1<tm1Msd> , Hemizygous for Tg(SMN1-SMN2*)16Cll

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Also Known As:SMN2;SMNRT;Smn-

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Expression Data

Control Suggestions

Additional Information

Selected References

Grm7Tg(SMN2)89Ahmb

Allele Symbol: Grm7Tg(SMN2)89Ahmb

Smn1tm1Msd

Allele Symbol: Smn1tm1Msd

Tg(SMN1-SMN2*)16Cll

Allele Symbol: Tg(SMN1-SMN2*)16Cll

Disease Terms

Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Genotype: Smn1tm1Msd related

Mammalian Phenotype Terms by Genotype

Genotype: Smn1tm1Msd/Smn1tm1Msd Tg(SMN1-SMN2*)16Cll/0 Grm7Tg(SMN2)89Ahmb/Grm7Tg(SMN2)89Ahmbinvolves: 129P2/OlaHsd * C57BL/6 * FVB/N

behavior/neurological phenotype

growth/size/body region phenotype

integument phenotype

mammalian phenotype

mortality/aging

muscle phenotype

nervous system phenotype

cardiovascular system phenotype

cellular phenotype

References

Additional - Grm7Tg(SMN2)89Ahmb related

Additional - Smn1tm1Msd related

Additional - Tg(SMN1-SMN2*)16Cll related

Genotyping Protocols

Breeding Considerations

Citation

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Live Mouse

Cryorecovery - Pricing

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Additional Use Restrictions Apply

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Also Known As:SMN2;SMN^RT;Smn-

Grm7^{Tg(SMN2)89Ahmb}

Allele Symbol: Grm7^{Tg(SMN2)89Ahmb}

Smn1^tm1Msd

Allele Symbol: Smn1^tm1Msd

Genotype: Smn1^tm1Msd related

Genotype: Smn1^tm1Msd/Smn1^tm1Msd Tg(SMN1-SMN2)16Cll/0 Grm7^{Tg(SMN2)89Ahmb}/Grm7^{Tg(SMN2)89Ahmb}
involves: 129P2/OlaHsd C57BL/6 * FVB/N

Additional - Grm7^{Tg(SMN2)89Ahmb} related

Additional - Smn1^tm1Msd related