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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Gdf2tm1Lex
targeted mutation 1, Lexicon Genetics
MGI:5703975
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Gdf2tm1Lex/Gdf2tm1Lex involves: 129S5/SvEvBrd * C57BL/6 MGI:5708081
ht2
Gdf2tm1Lex/Gdf2+ involves: 129S5/SvEvBrd * C57BL/6 MGI:5708082


Genotype
MGI:5708081
hm1
Allelic
Composition
Gdf2tm1Lex/Gdf2tm1Lex
Genetic
Background
involves: 129S5/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gdf2tm1Lex mutation (1 available); any Gdf2 mutation (25 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Neutralization of BMP10 causes defective vascular development in Gdf2tm1Lex/Gdf2+ and Gdf2tm1Lex/Gdf2tm1Lex mice

cardiovascular system
N
• surprisingly, untreated homozygotes are viable and fertile and do not display any embryonic or early postnatal defects in vascular development
• overall morphology and density of the retinal vasculature is normal at P7
• similarly, neonatal tracheal blood vasculature and tracheal lymphatic vessels appear normal
• after treatment with anti-BMP10, neonatal homozygotes show a disorganized tracheal blood vasculature, unlike similarly treated wild-type controls
• after treatment with anti-BMP10 monoclonal antibody from P2 through P7, neonatal homozygotes display abnormal retinal vasculature, unlike similarly treated wild-type controls
• after treatment with anti-BMP10, retinal vascular density is markedly increased
• after treatment with anti-BMP10, affected retinal blood vessels show reduced coverage of alphaSMA-positive mural cells
• after treatment with anti-BMP10, expansion of the vascular plexus in the nerve fiber layer from the optic nerve head (ONH) is markedly delayed

immune system
• after treatment with anti-BMP10, P7 tracheal lymphatic vessels appear highly irregular
• after treatment with anti-BMP10, P7 tracheal lymphatic vessels appear dilated

vision/eye
• after treatment with anti-BMP10 monoclonal antibody from P2 through P7, neonatal homozygotes display abnormal retinal vasculature, unlike similarly treated wild-type controls
• after treatment with anti-BMP10, retinal vascular density is markedly increased
• after treatment with anti-BMP10, affected retinal blood vessels show reduced coverage of alphaSMA-positive mural cells
• after treatment with anti-BMP10, expansion of the vascular plexus in the nerve fiber layer from the optic nerve head (ONH) is markedly delayed




Genotype
MGI:5708082
ht2
Allelic
Composition
Gdf2tm1Lex/Gdf2+
Genetic
Background
involves: 129S5/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gdf2tm1Lex mutation (1 available); any Gdf2 mutation (25 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Neutralization of BMP10 causes defective vascular development in Gdf2tm1Lex/Gdf2+ and Gdf2tm1Lex/Gdf2tm1Lex mice

cardiovascular system
• after treatment with anti-BMP10 monoclonal antibody from P2 through P7, heterozygotes show less severe defects in retinal vasculature relative to similarly treated homozygotes
• after treatment with anti-BMP10, retinal vascular density is increased to a lesser extent than in similarly treated homozygotes
• however, untreated heterozygotes exhibit normal retinal vasculature

vision/eye
• after treatment with anti-BMP10 monoclonal antibody from P2 through P7, heterozygotes show less severe defects in retinal vasculature relative to similarly treated homozygotes
• after treatment with anti-BMP10, retinal vascular density is increased to a lesser extent than in similarly treated homozygotes
• however, untreated heterozygotes exhibit normal retinal vasculature





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last database update
11/12/2024
MGI 6.24
The Jackson Laboratory