About   Help   FAQ
Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Hif1atm1Pec
targeted mutation 1, Peter Carmeliet
MGI:2179429
Summary 4 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Hif1atm1Pec/Hif1atm1Pec involves: 129S6/SvEvTac MGI:3618336
hm2
Hif1atm1Pec/Hif1atm1Pec involves: 129X1/SvJ * Swiss MGI:3615378
cx3
Egln2tm1Pec/Egln2tm1Pec
Hif1atm1Pec/Hif1a+
involves: 129S/SvEv * Swiss MGI:3777337
cx4
Egln3tm1Pjr/Egln3tm1Pjr
Hif1atm1Pec/Hif1a+
involves: 129S/SvEv * Swiss MGI:3798395


Genotype
MGI:3618336
hm1
Allelic
Composition
Hif1atm1Pec/Hif1atm1Pec
Genetic
Background
involves: 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1atm1Pec mutation (0 available); any Hif1a mutation (48 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
embryo
• E9.5 embryos display developmental arrest and morphological phenotypes identical to those previously reported for other genetic backgrounds




Genotype
MGI:3615378
hm2
Allelic
Composition
Hif1atm1Pec/Hif1atm1Pec
Genetic
Background
involves: 129X1/SvJ * Swiss
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1atm1Pec mutation (0 available); any Hif1a mutation (48 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• embryos with cardia bifida die around E9.5-E10

growth/size/body
• growth retarded after E8.5
• embryos with heart looping defects are less retarded than embryos with cardia bifida

cardiovascular system
• embryonic angiogenesis is impaired, however differentiation of angioblasts to endothelial cells and their subsequent assembly into a primary vascular labyrinth in the yolk sac and embryo proper at E8.5 occurs, indicating that vasculogenesis occurs
• distal dorsal aorta is regressed in homozygotes but not wild-type
• vitelline artery and distal dorsal aorta are regressed in homozygotes but not wild-type
• myocardial trabeculation is significantly retarded in half or absent in the other half of E9.5 embryos, however cardiomyocytes differentiate normally in E9.5 embryos
• myocardial trabeculation is absent in half of E9.5 embryos
• cardiac development at E9.5 is severely abnormal
• in embryos that do form a single heart tube, primitive hearts fail to loop at all or looping occurs abnormally
• about 32% exhibit cardia bifida as the cardiac crescent fails to form and results in the development of two separate myocardial tubes, each lined by endocardial cells
• defective ventricle formation

embryo
• neural crest cells are abnormally distributed as early as E8.75, indicating impaired migration
• defective formation of pharyngeal arches
• the second pharyngeal arch is either small or absent
• the second pharyngeal arch is either small or absent
• growth retarded after E8.5
• embryos with heart looping defects are less retarded than embryos with cardia bifida
• head folds fail to close at E9.5
• remodeling of the immature capillary plexus into a mature vascular bed is disturbed

nervous system
• head folds fail to close at E9.5

craniofacial
• defective formation of pharyngeal arches
• the second pharyngeal arch is either small or absent
• the second pharyngeal arch is either small or absent

muscle
• myocardial trabeculation is significantly retarded in half or absent in the other half of E9.5 embryos, however cardiomyocytes differentiate normally in E9.5 embryos
• myocardial trabeculation is absent in half of E9.5 embryos

homeostasis/metabolism
• E8.5 embryos cannot survive for more than 6-10 hours in normoxic, normoglycemic culture conditions (wildtype survive for at least 24 hours)
• hyperoxic culture conditions partially rescue cardiac development and prolong survival or homozygous embryos to E9.25-9.5, but not neural crest development and vascular remodeling

cellular
• vitelline artery and distal dorsal aorta are regressed in homozygotes but not wild-type
• neural crest cells are abnormally distributed as early as E8.75, indicating impaired migration




Genotype
MGI:3777337
cx3
Allelic
Composition
Egln2tm1Pec/Egln2tm1Pec
Hif1atm1Pec/Hif1a+
Genetic
Background
involves: 129S/SvEv * Swiss
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Egln2tm1Pec mutation (0 available); any Egln2 mutation (18 available)
Hif1atm1Pec mutation (0 available); any Hif1a mutation (48 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
muscle
N
• double mutants show ischemic muscle damage that is intermediate to Egln2/Epas1 double mutants and Egln2-null mice, so protection is partially lost in these animals




Genotype
MGI:3798395
cx4
Allelic
Composition
Egln3tm1Pjr/Egln3tm1Pjr
Hif1atm1Pec/Hif1a+
Genetic
Background
involves: 129S/SvEv * Swiss
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Egln3tm1Pjr mutation (0 available); any Egln3 mutation (24 available)
Hif1atm1Pec mutation (0 available); any Hif1a mutation (48 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• the number of neurons is similar to that in mice homozygous for Egln3tm1Pjr alone
• the nerve growth factor dose-response survival curve of superior cervical ganglia neurons is not significantly different from that of neurons homozygous for Egln3tm1Pjr alone





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
Citing These Resources
Funding Information
Warranty Disclaimer, Privacy Notice, Licensing, & Copyright
Send questions and comments to User Support.
last database update
04/23/2024
MGI 6.23
The Jackson Laboratory