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Nf1 expression is dependent on strain background: implications for tumor suppressor haploinsufficiency studies

Affiliation

  • 1 Mouse Cancer Genetics Program, National Cancer Institute-Frederick, West 7th Street at Fort Detrick, P.O. Box B, Building 560, Rm 31-20, Frederick, MD 21702, USA.
  • PMID: 17216419
  • PMCID: PMC6687394
  • DOI: 10.1007/s10048-006-0078-5

Free PMC article

Nf1 expression is dependent on strain background: implications for tumor suppressor haploinsufficiency studies

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Authors

Affiliation

  • 1 Mouse Cancer Genetics Program, National Cancer Institute-Frederick, West 7th Street at Fort Detrick, P.O. Box B, Building 560, Rm 31-20, Frederick, MD 21702, USA.
  • PMID: 17216419
  • PMCID: PMC6687394
  • DOI: 10.1007/s10048-006-0078-5

Abstract

Neurofibromatosis type 1 (NF1) is the most common cancer predisposition syndrome affecting the nervous system, with elevated risk for both astrocytoma and peripheral nerve sheath tumors. NF1 is caused by a germline mutation in the NF1 gene, with tumors showing loss of the wild type copy of NF1. In addition, NF1 heterozygosity in surrounding stroma is important for tumor formation, suggesting an additional role of haploinsufficiency for NF1. Studies in mouse models and NF1 families have implicated modifier genes unlinked to NF1 in the severity of the disease and in susceptibility to astrocytoma and peripheral nerve sheath tumors. To determine if differences in Nf1 expression may contribute to the strain-specific effects on tumor predisposition, we examined the levels of Nf1 gene expression in mouse strains with differences in tumor susceptibility using quantitative polymerase chain reaction. The data presented in this paper demonstrate that strain background has as much effect on Nf1 expression levels as mutation of one Nf1 allele, indicating that studies of haploinsufficiency must be carefully interpreted with respect to strain background. Because expression levels do not correlate entirely with the susceptibility or resistance to tumors observed in the strain, these data suggest that either variation in Nf1 levels is not responsible for the differences in astrocytoma and peripheral nerve sheath tumor susceptibility in Nf1-/+;Trp53-/+cis mice, or that certain mouse strains have evolved compensatory mechanisms for differences in Nf1 expression.

Figures

Comparison of nerve sheath tumor…

Comparison of nerve sheath tumor resistance loci, Nstr1 and Nstr2 , to quantitative…

Standard PCR annealing temperature gradients…

Standard PCR annealing temperature gradients from 50 to 70°C using Nf1 primer set…

qPCR of Nf1 ( a…

qPCR of Nf1 ( a ) and Nf1 exon 9a ( b )…

qPCR of Nf1 expression levels…

qPCR of Nf1 expression levels in the brains of astrocytoma susceptible ( susc…

Neurofibromatosis type 1 (NF1) is the most common cancer predisposition syndrome affecting the nervous system, with elevated risk for both astrocytoma and peripheral nerve sheath tumors. NF1 is caused by a germline mutation in the NF1 gene, with tumors showing loss of the wild type copy of NF1. In a …

Overview

Also Known As:Nf1flox

These Nf1 flox mice possess loxP sites flanking exons 31-32 of the neurofibromatosis 1 gene (Nf1), and have applications in studying cancer, neural crest development and neurofibromatosis type I.

Donating Investigator

Luis F Parada, UT Southwestern Medical Center

Genetic overview

Genetic Background Generation

Nf1 tm1Par

Allele Type Gene Symbol Gene Name
Targeted (Conditional ready (e.g. floxed), No functional change) Nf1 neurofibromin 1

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Research Applications

  • Neurobiology Research
  • Research Tools
  • Mouse/Human Gene Homologs
  • Cancer Research

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Base Price

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

Mutation in the human neurofibromin gene, NF1, is the cause of the autosomal dominant disorder Type I Neurofibromatosis. These mice possess loxP sites on either side of exons 31 and 32 of the targeted gene. 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 exons 31 and 32 deleted in the cre-expressing tissue(s).

When bred to a strain with Cre recombinase expression in the developing neural tube (see Stock No. 009107 for example), this mutant mouse strain may be useful in studies of Type I Neurofibromatosis.

When bred to a strain with Cre recombinase expression in neuronal cells (see Stock No. 003966 for example), this mutant mouse strain may be useful in studies of cerebral cortex development and reactive astrogliosis.

When bred to a strain with Cre recombinase expression in endothelial cells (see Stock No. 008863 for example), this mutant mouse strain may be useful in studies of neural crest development.

When bred to B6.Cg-Tg(Prrx1-cre)1Cjt/J mice (Stock No. 005584), mesenchyme-specific cre-expression results in mice that exhibit an increase in the amount of connective tissue, as well as muscle dystrophy characterized by fibrosis, a reduced number of muscle fibers, and reduced muscle force.

When bred to mice carrying Tg(Mx1-cre)1Cgn (Stock No. 003556), interferon-induced Cre-mediated recombination results in a progressive myeloproliferative disorder.

This allele is also part of the MADM-TG,p53KO,NF1-flox strain (Stock No. 017530), which is a genetic mosaicism model for cancer.

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. This is the case for the strain above. 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.

Development

A targeting vector containing a loxP site and a PGKNeo cassette was inserted upstream of exon 31. A second loxP site was inserted downstream of exon 32. The construct was electroporated into 129 derived R1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric animals were crossed to C57BL/6 mice. The mice were then crossed to several other mutant lines. The combination mutant strain, with a mix of CD1, C57BL/6 and 129 genetic backgrounds, was crossed to C57BL/6J to separate the Nf1 tm1Par allele.

Control Suggestions

Approximate Controls
  • 000664 C57BL/6J
  • 101045 B6129SF2/J

Additional Information

Selected References
  • Liu C; Sage JC; Miller MR; Verhaak RG; Hippenmeyer S; Vogel H; Foreman O; Bronson RT; Nishiyama A; Luo L; Zong H. 2011. Mosaic analysis with double markers reveals tumor cell of origin in glioma. Cell 146(2):209-21PubMed: 21737130MGI: J:174616
  • Zhu Y; Romero MI; Ghosh P; Ye Z; Charnay P; Rushing EJ; Marth JD; Parada LF. 2001. Ablation of NF1 function in neurons induces abnormal development of cerebral cortex and reactive gliosis in the brain. Genes Dev 15(7):859-76PubMed: 11297510MGI: J:68558

View All References

Genetics

Nf1 tm1Par

Allele Symbol: Nf1 tm1Par

Steven McKinnon, UT Southwestern Medical Center

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
  • juvenile myelomonocytic leukemia
  • neurofibromatosis

Research Areas By Phenotype

This mouse can be used to support research in many areas including:
  • Neurobiology Research
    • Cre-lox System
      • loxP-flanked Sequences
  • Research Tools
    • Cre-lox System
      • loxP-flanked Sequences
  • Mouse/Human Gene Homologs
    • Neurofibromatosis Type I
  • Cancer Research
    • Increased Tumor Incidence
      • Other Tissues/Organs: brain

Mammalian Phenotype Terms by Genotype

Genotype: Nf1 tm1Par /Nf1 tm1Par Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL

cardiovascular system phenotype
  • double outlet right ventricle
    • seen in 8 of 11 embryos (MGI Ref ID J:80323)
  • pericardial effusion
      (MGI Ref ID J:80323)
  • thin myocardium
    • 8 of 11 embryos exhibit a thinned myocardium (MGI Ref ID J:80323)
  • thin myocardium compact layer
      (MGI Ref ID J:80323)
  • ventricular septal defect
    • 10 of 11 embryos exhibit ventricular septal defects (MGI Ref ID J:80323)
  • increased atrioventricular cushion size
    • 8 of 11 embryos show an enlarged atrioventricular cushion (MGI Ref ID J:80323)
homeostasis/metabolism phenotype
    pericardial effusion
      (MGI Ref ID J:80323)
muscle phenotype
  • thin myocardium
    • 8 of 11 embryos exhibit a thinned myocardium (MGI Ref ID J:80323)
  • thin myocardium compact layer
      (MGI Ref ID J:80323)

Genotype: Nf1 tm1Par /Nf1 tm1Par Tg(Prrx1-cre)1Cjt/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * C57BL/6N * SJL/J

hematopoietic system phenotype
  • increased osteoclast cell number
    • callus following fracture shows increased number of osteoclasts; most osteoclasts are localized within fibrous tissue and not on the bone surface as in controls (MGI Ref ID J:193350)
homeostasis/metabolism phenotype
  • abnormal bone healing
    • accumulation and persistence of fibrous tissue in the fracture gap, with increased numbers of osteoclasts (MGI Ref ID J:193350)
    • ectopic fat tissue is seen in the fracture site (MGI Ref ID J:193350)
    • hat bony bridging is not observed (MGI Ref ID J:193350)
    • while total callus volume following fracture is larger in mutants at day 7 and 10 due to rapid initial growth of fibrous tissue (desmal type ossification), by day 14 and 21, the total callus volume is significantly smaller (MGI Ref ID J:193350)
    • increase in number of blood vessels in mutant fractures (in callus) compared to controls, indicating increased vascularization of the fracture tissue, however no osteogenesis results from this increased vascularization (MGI Ref ID J:193350)
    • mutants exhibit delayed and defective fracture healing characterized by diminished cartilaginous callus formation, increased bone formation near the cortical bone on the periosteum but not in the fracture gap, and persistence of cartilage at day 21 such that bony bridging is not observed (MGI Ref ID J:193350)
immune system phenotype
  • increased osteoclast cell number
    • callus following fracture shows increased number of osteoclasts; most osteoclasts are localized within fibrous tissue and not on the bone surface as in controls (MGI Ref ID J:193350)
skeleton phenotype
  • abnormal bone healing
    • accumulation and persistence of fibrous tissue in the fracture gap, with increased numbers of osteoclasts (MGI Ref ID J:193350)
    • hat bony bridging is not observed (MGI Ref ID J:193350)
    • increase in number of blood vessels in mutant fractures (in callus) compared to controls, indicating increased vascularization of the fracture tissue, however no osteogenesis results from this increased vascularization (MGI Ref ID J:193350)
    • ectopic fat tissue is seen in the fracture site (MGI Ref ID J:193350)
    • while total callus volume following fracture is larger in mutants at day 7 and 10 due to rapid initial growth of fibrous tissue (desmal type ossification), by day 14 and 21, the total callus volume is significantly smaller (MGI Ref ID J:193350)
    • mutants exhibit delayed and defective fracture healing characterized by diminished cartilaginous callus formation, increased bone formation near the cortical bone on the periosteum but not in the fracture gap, and persistence of cartilage at day 21 such that bony bridging is not observed (MGI Ref ID J:193350)
  • abnormal cartilage morphology
    • bone fractures exhibit impaired cartilage formation and increased periosteal ossification at the cortices (MGI Ref ID J:193350)
  • increased compact bone volume
    • dramatic cortical bone thickening following fracture (MGI Ref ID J:193350)
  • decreased bone mineral density
    • decrease of regenerative tissue bone mineral density following fracture (MGI Ref ID J:193350)
  • abnormal osteoblast cell number
    • fewer osteoblasts are seen within the fracture gap throughout healing compared to controls, however, osteoblast number is increased at the periosteal surface (MGI Ref ID J:193350)
  • fragile skeleton
    • fractured bones of mutants that are allowed to heal also exhibit a lower torsional stiffness and ultimate torque at failure compared to controls (MGI Ref ID J:193350)
    • bones are weaker; femora show lower torsional stiffness and ultimate torque at failure compared to controls (MGI Ref ID J:193350)
  • abnormal endochondral bone ossification
    • endochondrial formation is impaired following fracture but periosteal bone formation is enhanced (MGI Ref ID J:193350)
  • increased osteoid thickness
    • thickening of the osteoid layer in the periosteal region following fracture (MGI Ref ID J:193350)
  • increased osteoclast cell number
    • callus following fracture shows increased number of osteoclasts; most osteoclasts are localized within fibrous tissue and not on the bone surface as in controls (MGI Ref ID J:193350)
  • abnormal osteoid morphology
    • presence of large areas of non-mineralized osteoid in the fracture gap, indicating decreased mineralization of the extracellular matrix (MGI Ref ID J:193350)

Genotype: Nf1 tm1Par /Nf1 tm1Par Tg(Prrx1-cre)1Cjt/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * SJL/J

cellular phenotype
  • abnormal myoblast differentiation
    • maker analysis indicates a severe disruption of myoblast terminal differentiation (MGI Ref ID J:173779)
  • increased myoblast proliferation
    • marker analysis indicates that migration and proliferation of pre-muscle cells at E11.5 are normal but increased proliferation of myoblasts in ventral muscle masses is seen (MGI Ref ID J:173779)
growth/size/body region phenotype
  • decreased body weight
    • weight is on average reduced by 25% (MGI Ref ID J:173779)
limbs/digits/tail phenotype
  • short limbs
    • short-limbed dwarfism, with mutants showing a reduction in entire limb size (MGI Ref ID J:173779)
muscle phenotype
  • abnormal muscle development
    • the m. latissimus dorsi appears smaller and shows rarefaction of muscle fibers (MGI Ref ID J:173779)
    • marker analysis indicates a defect in muscle formation at E13.5, with specific muscle primordial reduced in size or entirely missing; approximate 30% reduction in the m. triceps size and about 50% reduction in the m. gluteus maximus size of E13.5 embryos (MGI Ref ID J:173779)
    • distal muscle groups in the extremities are most affected, with some muscles completely missing, indicating that the muscle differentiation process is disturbed (MGI Ref ID J:173779)
  • abnormal muscle morphology
    • muscle fibers are thinned out at E16.5 (MGI Ref ID J:173779)
    • large areas of dystrophic musculature are occupied by fat tissue (MGI Ref ID J:173779)
    • muscle connective tissue shows increased proliferation at E14.5 and an increase in connective tissue in muscles is already seen at E16.5 (MGI Ref ID J:173779)
    • mutants exhibit muscle dystrophy (MGI Ref ID J:173779)
  • decreased skeletal muscle mass
    • reduction in muscle size and mass (MGI Ref ID J:173779)
  • skeletal muscle fibrosis
    • generalized muscle fibrosis, characterized by expansion of collagen-rich connective tissue, and reduction in total number of muscle fibers (MGI Ref ID J:173779)
  • abnormal muscle fiber morphology
    • muscles show a 20% increase in the number of fibers with cleft-like invaginations (split fibers) (MGI Ref ID J:173779)
    • muscle fiber size appears more variable than in controls, however no overt muscle regeneration is seen (MGI Ref ID J:173779)
  • decreased skeletal muscle fiber number
    • total number of muscle fibers is reduced by 50% in the triceps (MGI Ref ID J:173779)
  • abnormal myoblast differentiation
    • maker analysis indicates a severe disruption of myoblast terminal differentiation (MGI Ref ID J:173779)
  • decreased muscle weight
    • weight of triceps muscle is reduced by more than 50% (MGI Ref ID J:173779)
  • abnormal muscle physiology
    • in the force gauge pull test, mice show a dramatic reduction in muscle force (MGI Ref ID J:173779)
    • satellite cells exhibit normal self-renewal but impaired differentiation as indicated by diminished myotube formatio (MGI Ref ID J:173779)
  • abnormal myogenesis
    • defect in myogenesis affecting the terminal differentiation of myoblasts between E12.5 and E14.5 (MGI Ref ID J:173779)
  • increased myoblast proliferation
    • marker analysis indicates that migration and proliferation of pre-muscle cells at E11.5 are normal but increased proliferation of myoblasts in ventral muscle masses is seen (MGI Ref ID J:173779)

Genotype: Nf1 tm1Par /Nf1 tm1Par Tg(Mx1-cre)1Cgn/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

behavior/neurological phenotype
  • abnormal gait
    • pIpC injected mice at 3 to 5 days of age exhibit hunching by 5-6 months of age (MGI Ref ID J:90973)
  • hunched posture
    • pIpC injected mice at 3 to 5 days of age exhibit abnormal gait by 5-6 months of age (MGI Ref ID J:90973)
immune system phenotype
  • abnormal myeloid leukocyte morphology
    • pIpC injected mice at 3 to 5 days of age exhibit elevated numbers of differentiated myeloid cells by 3 months of age (MGI Ref ID J:90973)
  • increased neutrophil cell number
    • pIpC injected mice at 3 to 5 days of age exhibit increased numbers of morphologically normal neutrophils by 3 months of age (MGI Ref ID J:90973)
  • increased granulocyte number
    • pIpC injected mice show an increase in numbers of differentiated granulocytic cells (MGI Ref ID J:90973)
  • increased leukocyte cell number
    • cultures from pIpC injected mice show an increase in the percentage of monocyte-macrophage cells (MGI Ref ID J:90973)
    • pIpC injected mice at 3 to 5 days of age exhibit elevated leukocyte counts by 3 months of age (MGI Ref ID J:90973)
  • abnormal myelopoiesis
    • spleen from pIpC injected mice shows a massive increase in myelopoiesis (MGI Ref ID J:90973)
  • increased monocyte cell number
    • pIpC injected mice show an increase in numbers of immature monocytic cells in the bone marrow (MGI Ref ID J:90973)
    • pIpC injected mice at 3 to 5 days of age exhibit increased numbers of morphologically normal monocytes by 3 months of age (MGI Ref ID J:90973)
  • abnormal spleen morphology
    • spleens from pIpC injected mice contain large numbers of CFU-GM (MGI Ref ID J:90973)
  • enlarged spleen
    • pIpC injected mice at 3 to 5 days of age exhibit progressive splenomegaly with extensive infiltration of myeloid cells at various stages of maturation (MGI Ref ID J:90973)
  • increased lymphocyte cell number
    • pIpC injected mice at 3 to 5 days of age exhibit increased numbers of morphologically normal lymphocytes by 3 months of age (MGI Ref ID J:90973)
growth/size/body region phenotype
  • enlarged spleen
    • pIpC injected mice at 3 to 5 days of age exhibit progressive splenomegaly with extensive infiltration of myeloid cells at various stages of maturation (MGI Ref ID J:90973)
integument phenotype
  • disheveled coat
    • pIpC injected mice at 3 to 5 days of age have a disheveled appearance by 5-6 months of age (MGI Ref ID J:90973)
mortality/aging
  • premature death
    • 50% of pIpC treated mice die by 7.5 months of age (MGI Ref ID J:90973)
hematopoietic system phenotype
  • abnormal bone marrow cell morphology/development
    • bone marrow from pIpC injected mice contains elevated numbers of CFU-GM and an increase in the numbers of CFU-GM that are hypersensitive to granulocyte-macrophage colony stimulating factor (GM-CSF) and CFU-GM colonies are larger than normal and show abnormal spreading morphology (MGI Ref ID J:90973)
    • increase in numbers of immature monocytic cells in the bone marrow of pIpC treated mice (MGI Ref ID J:90973)
    • bone marrow from pIpC injected mice is highly cellular, comprised of myeloid cells at various stages of differentiation (MGI Ref ID J:90973)
    • apoptosis is reduced in the bone marrow of pIpC injected mice (MGI Ref ID J:90973)
    • mal spreading morphology (MGI Ref ID J:90973)
  • abnormal myelopoiesis
    • spleen from pIpC injected mice shows a massive increase in myelopoiesis (MGI Ref ID J:90973)
  • increased lymphocyte cell number
    • pIpC injected mice at 3 to 5 days of age exhibit increased numbers of morphologically normal lymphocytes by 3 months of age (MGI Ref ID J:90973)
  • increased monocyte cell number
    • pIpC injected mice show an increase in numbers of immature monocytic cells in the bone marrow (MGI Ref ID J:90973)
    • pIpC injected mice at 3 to 5 days of age exhibit increased numbers of morphologically normal monocytes by 3 months of age (MGI Ref ID J:90973)
  • enlarged spleen
    • pIpC injected mice at 3 to 5 days of age exhibit progressive splenomegaly with extensive infiltration of myeloid cells at various stages of maturation (MGI Ref ID J:90973)
  • increased neutrophil cell number
    • pIpC injected mice at 3 to 5 days of age exhibit increased numbers of morphologically normal neutrophils by 3 months of age (MGI Ref ID J:90973)
  • abnormal myeloid leukocyte morphology
    • pIpC injected mice at 3 to 5 days of age exhibit elevated numbers of differentiated myeloid cells by 3 months of age (MGI Ref ID J:90973)
  • abnormal common myeloid progenitor cell morphology
    • myeloid progenitors from pIpC injected mice show increased proliferation (MGI Ref ID J:90973)
  • abnormal spleen morphology
    • spleens from pIpC injected mice contain large numbers of CFU-GM (MGI Ref ID J:90973)
  • abnormal definitive hematopoiesis
    • pIpC injected mice at 3 to 5 days of age develop overt signs of myeloproliferative disease beginning between 5 and 6 months of age (MGI Ref ID J:90973)
    • pIpC injected mice show a shift in hematopoiesis from the marrow to the spleen (MGI Ref ID J:90973)
  • increased leukocyte cell number
    • pIpC injected mice at 3 to 5 days of age exhibit elevated leukocyte counts by 3 months of age (MGI Ref ID J:90973)
    • cultures from pIpC injected mice show an increase in the percentage of monocyte-macrophage cells (MGI Ref ID J:90973)
  • increased granulocyte number
    • pIpC injected mice show an increase in numbers of differentiated granulocytic cells (MGI Ref ID J:90973)
  • abnormal hematopoietic cell number
    • pIpC injected mice at 3 to 5 days of age exhibit elevated numbers of differentiated lymphoid cells by 3 months of age (MGI Ref ID J:90973)

Genotype: Nf1 tm1Par /Nf1 tm1Par Tg(Syn1-cre)671Jxm/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

behavior/neurological phenotype
  • abnormal learning/memory/conditioning
    • mice display severe learning disability (MGI Ref ID J:68558)
growth/size/body region phenotype
  • decreased body weight
    • body weight and size are about 50% of normal (MGI Ref ID J:68558)
  • postnatal growth retardation
    • 3-4 days after birth, mice begin to exhibit growth retardation that is sustained into adulthood (MGI Ref ID J:68558)
mammalian phenotype
  • neoplasm
    • Normal – no evidence of tumors; optic gliomas, astrocytomas, or neurofibroma are not observed (MGI Ref ID J:68558)
nervous system phenotype
  • abnormal cerebral cortex morphology
    • increase in cell density in the cerebral cortex, often resulting in less apparent lamination (MGI Ref ID J:68558)
  • astrocytosis
    • mice display astrogliosis in various brain regions, however do not develop neuronal degeneration or microgliosis (MGI Ref ID J:68558)
  • decreased forebrain size
    • forebrain, but not the rest of the brain, is reduced in size, however mice exhibit normal neuronal development (MGI Ref ID J:68558)
  • thin cerebral cortex
    • about 20% reduction in coritcal thickness (MGI Ref ID J:68558)

Genotype: Nf1 tm1Par /Nf1 tm1Par Tg(Gfap-cre)77.6Mvs/0
involves: 129S1/Sv * 129X1/SvJ * BALB/c * C57BL/6NHsd

mammalian phenotype
  • neoplasm
    • Normal – mutants do not develop tumors (MGI Ref ID J:154673)

Genotype: Nf1 tm1Par /Nf1 tm1Par
involves: 129S1/Sv * 129X1/SvJ

nervous system phenotype
  • abnormal astrocyte physiology
    • astrocytes transfected with a cre-expresing adenovirus exhibit increased proliferation compared to in control cells (MGI Ref ID J:176586)

References

  • Liu C; Sage JC; Miller MR; Verhaak RG; Hippenmeyer S; Vogel H; Foreman O; Bronson RT; Nishiyama A; Luo L; Zong H. 2011. Mosaic analysis with double markers reveals tumor cell of origin in glioma. Cell 146(2):209-21PubMed: 21737130MGI: J:174616
  • Zhu Y; Romero MI; Ghosh P; Ye Z; Charnay P; Rushing EJ; Marth JD; Parada LF. 2001. Ablation of NF1 function in neurons induces abnormal development of cerebral cortex and reactive gliosis in the brain. Genes Dev 15(7):859-76PubMed: 11297510MGI: J:68558
tm1Par related’, ‘017639’)>”>Additional – Nf1 tm1Par related

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Genotyping Protocols

  • Separated MCA:Nf1
  • Separated PCR:Nf1
  • Genotyping resources and troubleshooting
  • Breeding Considerations

    When maintaining a live colony, these mice can be bred as homozygotes.

    Citation

    When using the Nf1flox mouse strain in a publication, please cite the originating article(s) and include JAX stock #017639 in your Materials and Methods section.

    Animal Health Reports

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

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    The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain’s phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

    Overview Also Known As:Nf1flox These Nf1 flox mice possess loxP sites flanking exons 31-32 of the neurofibromatosis 1 gene ( Nf1 ), and have applications in studying cancer, neural crest