Strain Name:

B6;129-Vegfatm4Pec/Mmjax

Availability:

Cryopreserved - Ready for recovery     Available at the JAX MMRRC

Please refer to the Mutant Mouse Regional Resource Center (MMRRC) for information about B6;129-Vegfatm4Pec/Mmjax MMRRC Stock Number 034406.
Retinal arterial development in VEGF188 mice is impaired. Homozygotes exhibit reduced fertility, smaller litter sizes and some prenatal lethality. This mutant mouse strain may be useful in studies of retinal angiogenesis.

Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Former Names B6;129-Vegfatm4Pec/Mmnc    (Changed: 01-AUG-11 )
Type Mutant Stock; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Specieslaboratory mouse
Generation+pN1
Generation Definitions
 
Donating Investigator Patricia D'Amore,   Schepens Eye Research Institute

Description

Heterozygote: Heterozygote phenotype is similar to the wild-type phenotype.

Homozygote: Mice homozygous for the targeted mutation are viable, but exhibit reduced fertility, smaller litter sizes and some prenatal lethality. Surviving homozygotes gain less weight than wild-type controls. Retinal arterial development in VEGF188 mice is impaired. By post natal day 5 (P5), only half the normal number of large vessels (mostly venules) are present in the vascular bed of the retina. By P9, arterioles are observed to be smaller in size and only 50% have developed and grown out over 17% of the retina. In controls, 88% of the retinal radius is covered by P9. Venous and capillary development appears normal. VEGF188 mice express a VEGF protein with all eight exons that avidly binds to the cell surface and extracellular matrix. This mutant mouse strain may be useful in studies of retinal angiogenesis.

Development
A targeting vector was designed to insert a loxP-flanked neomycin cassette into the 3' UTR of a cDNA containing fused exons 4 through 8. The construct was electroporated into (129X1/SvJ x 129S1/Sv)F1 derived R1 embryonic stem (ES) cells. Transient Cre expression in targeted cells excised the neo cassette. Correctly targeted ES cells were injected into blastocysts. The resulting chimeric animals were bred to C57BL/6 and then maintained by sibling mating. The VEGF188 isoform contains all 8 exons. Upon arrival, mice were bred to C57BL/6J for at least 1 generation to establish the colony.

Related Strains

Strains carrying other alleles of Vegfa
016971   B6.Cg-Vegfatm3.1Pec/Mmjax
016973   B6;129-Vegfatm1Pec/Mmjax
005705   FVB-Tg(KRT14-Vegfa)3Dtm/J
View Strains carrying other alleles of Vegfa     (3 strains)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).
DiGeorge Syndrome; DGS
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Microvascular Complications of Diabetes, Susceptibility to, 1; MVCD1   (VEGFA)
Vascular Endothelial Growth Factor A; VEGFA   (VEGFA)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

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

Vegfatm4Pec/Vegfatm4Pec

        involves: 129S1/Sv * 129X1/SvJ
  • mortality/aging
  • partial embryonic lethality during organogenesis   (MGI Ref ID J:75507)
    • about half die between E9.5 and E13.5 and the rest survive for prolonged periods after birth   (MGI Ref ID J:81698)
  • growth/size/body phenotype
  • decreased body weight
    • surviving mice gain less weight at 7 weeks of age   (MGI Ref ID J:75507)
  • cardiovascular system phenotype
  • abnormal blood vessel morphology
    • about 50% of neonates exhibit severe DiGeorge syndome-like vessel malformations   (MGI Ref ID J:81698)
    • vascular defects are so severe in 19% of embryos that they cause circulatory collapse by E13.5   (MGI Ref ID J:81698)
    • abnormal arteriole morphology
      • arterioles, but not venules, in the retina are smaller and extend over only 18% of the vascular bed (compared to 90% in controls)   (MGI Ref ID J:75507)
    • abnormal pharyngeal arch artery morphology
      • E14.5 embryos and neonates have remodeling defects of the 4th, 6th and, less frequently, 3rd pharyngeal arch arteries   (MGI Ref ID J:81698)
      • in E9.5 embryos, the arch arteries appear as primitive capillary networks, often with an irregular small lumen and signs of regression (19%)   (MGI Ref ID J:81698)
      • while the 3rd, 4th and 6th pharyngeal arch arteries are present by E10-10.5, subsequent malformations include hypoplasia, an irregular lumen size, and signs of regression in vessels that should normally persist   (MGI Ref ID J:81698)
      • abnormal fourth pharyngeal arch artery morphology
        • variable defects   (MGI Ref ID J:81698)
        • malformations of the 4th arch artery include a persistence of the carotid duct segment between the left carotid and subclavian artery and a descending aorta   (MGI Ref ID J:81698)
      • abnormal sixth pharyngeal arch artery morphology
        • variable defects   (MGI Ref ID J:81698)
      • abnormal third pharyngeal arch artery morphology
        • variable defects   (MGI Ref ID J:81698)
    • abnormal retinal vasculature morphology
      • at P9, only half the normal number of arterioles develop, they are smaller in size, and grow out over only 17% of the retina   (MGI Ref ID J:75507)
      • capillary pruning is decreased, resulting in a more dense capillary bed and a slight increase in the number of periendothelial cells per retinal cell   (MGI Ref ID J:75507)
    • abnormal vascular regression
      • exhibit signs of regression in vessels of the pharyngeal arch that should normally persist   (MGI Ref ID J:81698)
    • double aortic arch
      • malformations of the 4th arch artery include a double aortic arch   (MGI Ref ID J:81698)
    • interrupted aortic arch
      • malformations of the 4th arch artery include type-B left 4th aortic arch interruption   (MGI Ref ID J:81698)
    • persistent right dorsal aorta
      • about 10% of embryos exhibit a dominant right dorsal aorta   (MGI Ref ID J:81698)
    • pulmonary trunk hypoplasia
      • hypoplasia of the pulmonary trunk   (MGI Ref ID J:81698)
    • retroesophageal right subclavian artery
      • malformations of the 4th arch artery include retroesophageal right subclavian artery   (MGI Ref ID J:81698)
    • right aortic arch
      • malformations of the 4th arch artery include a right-sided aortic arch   (MGI Ref ID J:81698)
  • persistent truncus arteriosis   (MGI Ref ID J:81698)
  • ventricular septal defect
    • ventricular septal defect   (MGI Ref ID J:81698)
  • reproductive system phenotype
  • decreased litter size   (MGI Ref ID J:75507)
  • reduced fertility
    • fewer number of litters during 4 months   (MGI Ref ID J:75507)
  • vision/eye phenotype
  • abnormal retinal vasculature morphology
    • at P9, only half the normal number of arterioles develop, they are smaller in size, and grow out over only 17% of the retina   (MGI Ref ID J:75507)
    • capillary pruning is decreased, resulting in a more dense capillary bed and a slight increase in the number of periendothelial cells per retinal cell   (MGI Ref ID J:75507)
  • craniofacial phenotype
  • abnormal pharyngeal arch artery morphology
    • E14.5 embryos and neonates have remodeling defects of the 4th, 6th and, less frequently, 3rd pharyngeal arch arteries   (MGI Ref ID J:81698)
    • in E9.5 embryos, the arch arteries appear as primitive capillary networks, often with an irregular small lumen and signs of regression (19%)   (MGI Ref ID J:81698)
    • while the 3rd, 4th and 6th pharyngeal arch arteries are present by E10-10.5, subsequent malformations include hypoplasia, an irregular lumen size, and signs of regression in vessels that should normally persist   (MGI Ref ID J:81698)
    • abnormal fourth pharyngeal arch artery morphology
      • variable defects   (MGI Ref ID J:81698)
      • malformations of the 4th arch artery include a persistence of the carotid duct segment between the left carotid and subclavian artery and a descending aorta   (MGI Ref ID J:81698)
    • abnormal sixth pharyngeal arch artery morphology
      • variable defects   (MGI Ref ID J:81698)
    • abnormal third pharyngeal arch artery morphology
      • variable defects   (MGI Ref ID J:81698)
  • pharyngeal arch hypoplasia
    • the first three pharyngeal arches are hypoplastic in 19% of E9.5 embryos   (MGI Ref ID J:81698)
  • embryogenesis phenotype
  • abnormal pharyngeal arch artery morphology
    • E14.5 embryos and neonates have remodeling defects of the 4th, 6th and, less frequently, 3rd pharyngeal arch arteries   (MGI Ref ID J:81698)
    • in E9.5 embryos, the arch arteries appear as primitive capillary networks, often with an irregular small lumen and signs of regression (19%)   (MGI Ref ID J:81698)
    • while the 3rd, 4th and 6th pharyngeal arch arteries are present by E10-10.5, subsequent malformations include hypoplasia, an irregular lumen size, and signs of regression in vessels that should normally persist   (MGI Ref ID J:81698)
    • abnormal fourth pharyngeal arch artery morphology
      • variable defects   (MGI Ref ID J:81698)
      • malformations of the 4th arch artery include a persistence of the carotid duct segment between the left carotid and subclavian artery and a descending aorta   (MGI Ref ID J:81698)
    • abnormal sixth pharyngeal arch artery morphology
      • variable defects   (MGI Ref ID J:81698)
    • abnormal third pharyngeal arch artery morphology
      • variable defects   (MGI Ref ID J:81698)
  • pharyngeal arch hypoplasia
    • the first three pharyngeal arches are hypoplastic in 19% of E9.5 embryos   (MGI Ref ID J:81698)
  • respiratory system phenotype
  • *normal* respiratory system phenotype
    • neonates display normal pulmonary development   (MGI Ref ID J:77480)
  • cellular phenotype
  • abnormal vascular regression
    • exhibit signs of regression in vessels of the pharyngeal arch that should normally persist   (MGI Ref ID J:81698)
View Research Applications

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

Developmental Biology Research
Internal/Organ Defects
      vasculature

Reproductive Biology Research
Fertility Defects

Sensorineural Research
Eye Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Vegfatm4Pec
Allele Name targeted mutation 4, Peter Carmeliet
Allele Type Targeted
Common Name(s) VEGF188;
Mutation Made ByDr. Peter Carmeliet,   University of Leuven
Strain of Origin(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
Promoter Vegfa, vascular endothelial growth factor A, mouse, laboratory
Molecular Note Genomic sequence containing exons 4 through 8 was replaced with corresponding cDNA. The resultant allele lacks splice sites and thereby produces a single isoform with high receptor binding properties. The exclusive presence of this isoform was verified by quatitative RT-PCR. [MGI Ref ID J:75507]

Genotyping

Genotyping Information

Genotyping Protocols

Vegfatm4Pec, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Stalmans I; Ng YS; Rohan R; Fruttiger M; Bouche A; Yuce A; Fujisawa H; Hermans B; Shani M; Jansen S; Hicklin D; Anderson DJ; Gardiner T; Hammes HP; Moons L; Dewerchin M; Collen D; Carmeliet P; D'Amore PA. 2002. Arteriolar and venular patterning in retinas of mice selectively expressing VEGF isoforms. J Clin Invest 109(3):327-36. [PubMed: 11827992]  [MGI Ref ID J:75507]

Additional References

Vegfatm4Pec related

Compernolle V; Brusselmans K; Acker T; Hoet P; Tjwa M; Beck H; Plaisance S; Dor Y; Keshet E; Lupu F; Nemery B; Dewerchin M; Van Veldhoven P; Plate K; Moons L; Collen D; Carmeliet P. 2002. Loss of HIF-2alpha and inhibition of VEGF impair fetal lung maturation, whereas treatment with VEGF prevents fatal respiratory distress in premature mice. Nat Med 8(7):702-10. [PubMed: 12053176]  [MGI Ref ID J:77480]

Maes C; Stockmans I; Moermans K; Van Looveren R; Smets N; Carmeliet P; Bouillon R; Carmeliet G. 2004. Soluble VEGF isoforms are essential for establishing epiphyseal vascularization and regulating chondrocyte development and survival. J Clin Invest 113(2):188-99. [PubMed: 14722611]  [MGI Ref ID J:87618]

Ruiz de Almodovar C; Coulon C; Salin PA; Knevels E; Chounlamountri N; Poesen K; Hermans K; Lambrechts D; Van Geyte K; Dhondt J; Dresselaers T; Renaud J; Aragones J; Zacchigna S; Geudens I; Gall D; Stroobants S; Mutin M; Dassonville K; Storkebaum E; Jordan BF; Eriksson U; Moons L; D'Hooge R; Haigh JJ; Belin MF; Schiffmann S; Van Hecke P; Gallez B; Vinckier S; Chedotal A; Honnorat J; Thomasset N; Carmeliet P; Meissirel C. 2010. Matrix-binding vascular endothelial growth factor (VEGF) isoforms guide granule cell migration in the cerebellum via VEGF receptor Flk1. J Neurosci 30(45):15052-66. [PubMed: 21068311]  [MGI Ref ID J:166454]

Stalmans I; Lambrechts D; De Smet F; Jansen S; Wang J; Maity S; Kneer P; Von Der Ohe M; Swillen A; Maes C; Gewillig M; Molin DG; Hellings P; Boetel T; Haardt M; Compernolle V; Dewerchin M; Plaisance S; Vlietinck R; Emanuel B; Gittenberger-De Groot AC; Scambler P; Morrow B; Driscol DA; Moons L; Esguerra CV; Carmeliet G; Behn-Krappa A; Devriendt K; Collen D; Conway SJ; Carmeliet P. 2003. VEGF: A modifier of the del22q11 (DiGeorge) syndrome? Nat Med 9(2):173-82. [PubMed: 12539040]  [MGI Ref ID J:81698]

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