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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
F2rtm1Ajc
targeted mutation 1, Andrew J Connolly
MGI:1857306
Summary 9 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
F2rtm1Ajc/F2rtm1Ajc B6.129S4-F2rtm1Ajc MGI:3521663
hm2
F2rtm1Ajc/F2rtm1Ajc involves: 129S4/SvJae MGI:4946501
hm3
F2rtm1Ajc/F2rtm1Ajc involves: 129S4/SvJae * C57BL/6 MGI:3784848
hm4
F2rtm1Ajc/F2rtm1Ajc involves: 129S4/SvJae * C57BL/6J MGI:3521509
cx5
F2rtm1Ajc/F2rtm1Ajc
F5tm1Dgi/F5tm1Dgi
B6.Cg-F5tm1Dgi F2rtm1Ajc MGI:3521664
cx6
F2rtm1Ajc/F2rtm1Ajc
St14tm1Bug/St14tm1Bug
involves: 129P2/OlaHsd * 129S4/SvJae MGI:5440276
cx7
F2rtm1Ajc/F2rtm1Ajc
F2rl1tm1Cgh/F2rl1tm1Cgh
involves: 129S4/SvJae MGI:5440277
cx8
F2rtm1Ajc/F2rtm1Ajc
F2rl1tm1Cgh/F2rl1tm1Cgh
F2rl3tm1Cgh/F2rl3tm1Cgh
involves: 129S4/SvJae * C57BL/6 MGI:3784875
cx9
F2rtm1Ajc/F2rtm1Ajc
F2rl1tm1Cgh/F2rl1tm1Cgh
involves: 129S4/SvJae * C57BL/6 MGI:3784874


Genotype
MGI:3521663
hm1
Allelic
Composition
F2rtm1Ajc/F2rtm1Ajc
Genetic
Background
B6.129S4-F2rtm1Ajc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
F2rtm1Ajc mutation (2 available); any F2r mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• urinary Na+ excretion was enhanced
• urinary DPD (degradation products of collagen I) concentration in homozygous mutant mice is reduced

limbs/digits/tail
• small, albeit significant, increase in femur length

mortality/aging
• by E12.5, 52% of mutant embryos are dead with extensive bleeding; the remaining embryos survive to adulthood and appear grossly normal

neoplasm
N
• when injected with B16-F10 melanoma cells via tail vein, homozygotes show no differences in hematogenous metastasis (tumor count or burden) relative to wild-type mice, indicating no protection against metastasis in this model

skeleton
N
• osteoblast number and surface are not significantly different between controls and mutant mice
• no changes in osteoclast number and surface
• small, albeit significant, increase in femur length
• diaphyseal endocortical volume is increased
• endocortical and cortical volumes are significantly increased
• trabecular bone volume fraction in the distal metaphyseal bone compartment is elevated
• significantly increased trabecular bone volume in the femoral metaphysis and diaphysis
• diaphyseal thickness was reduced
• trabecular separation is decreased

cardiovascular system
• at E8.75 to E10.5, embryos with gross bleeding are pale and display a disorganized yolk sac vasculature or delayed remodeling
• at E12.5, mutant yolk sacs lack blood-filled vessels
• at E9.5, 2 out of 3 mutant embryos exhibit a defect in the wall of the sinus venosus that is large enough to allow blood cells into the pericardial cavity
• at E9.5, hemorrhagic embryos often display a dilated pericardial sac, indicating cardiovascular failure
• at this stage, 4 out of 19 mutant embryos with microscopic bleeding display normal pericardial sacs
• by E9.5, ~66% of mutant embryos display microscopic bleeding in the pericardial and/or peritoneal, amniotic, and/or exocoelomic cavity
• live E9.5 to E10.5 embryos with both gross bleeding and vigorous heart beats are occasionally observed
• at E9.5, 22% of mutant embryos exhibit hemorrhage in the exocoelomic and/or pericardial cavities

cellular
• relative to wild-type, mutant endothelial cells display a 20-30% reduction in F10 (coagulation protease factor Xa)-triggered phosphoinositide hydrolysis
• a similar reduction is observed when ERK1/2 phosphorylation is used to assess F10 signaling
• in contrast, mutant lung fibroblasts exhibit a complete absence of F10-induced phosphoinositide hydrolysis
• cortical neurons from mutant fetuses exhibit a complete loss of activated protein C (APC)-mediated neuronal protection against NMDA-induced apoptosis

embryo
• at E8.75 to E10.5, embryos with gross bleeding are pale and display a disorganized yolk sac vasculature or delayed remodeling
• at E12.5, mutant yolk sacs lack blood-filled vessels
• at E9.5, mutant embryos show a variable developmental delay but no gross vascular anomalies

growth/size/body
• at E9.5, mutant embryos show a variable developmental delay but no gross vascular anomalies

nervous system
• cortical neurons from mutant fetuses exhibit a complete loss of activated protein C (APC)-mediated neuronal protection against NMDA-induced apoptosis

homeostasis/metabolism
N
• urinary Ca2+ excretion is not affected
• serum Ca2+ concentration is not affected
• serum Na+ and K+ values appear similar to controls
• at E9.5, 22% of mutant embryos exhibit hemorrhage in the exocoelomic and/or pericardial cavities
• serum RANKL level is significantly decreased, and the OPG level is increased, resulting in a significantly reduced RANKL/OPG ratio
• urinary Na+ excretion was enhanced
• serum RANKL level is significantly decreased
• serum osteoprotegerin (OPG) level is increased
• urinary DPD (degradation products of collagen I) concentration in homozygous mutant mice is reduced




Genotype
MGI:4946501
hm2
Allelic
Composition
F2rtm1Ajc/F2rtm1Ajc
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
F2rtm1Ajc mutation (2 available); any F2r mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• ~50% of homozygotes die between E9.0-10.0

limbs/digits/tail
• occasional




Genotype
MGI:3784848
hm3
Allelic
Composition
F2rtm1Ajc/F2rtm1Ajc
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
F2rtm1Ajc mutation (2 available); any F2r mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• the gallbladder fails to exhibit a normal short-circuit current response when stimulated with TFLLRN-NH2 and thrombin
• however, the short-circuit response to SLIGRL-NH2 and trypsin is normal

immune system
N
• mice exhibit a normal response to endotoxin treatment




Genotype
MGI:3521509
hm4
Allelic
Composition
F2rtm1Ajc/F2rtm1Ajc
Genetic
Background
involves: 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
F2rtm1Ajc mutation (2 available); any F2r mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• about 50% of homozygotes die between E9.0-10.0

embryo
• at E9.0-E9.5, homozygotes display a global developmental delay
• however, those that survive past E9.0-E10.0 catch up with control embryos by E11.5 and develop normally to birth
• starting at E9.0, mutant embryos become uniformly smaller than wild-type embryos
• at E9.0-E9.5, homozygotes display a delay in placental development

cardiovascular system
• by E9.5, approximately half of the mutant embryos display no heart beat
• however, E8.5 mutant embryos have beating hearts and a functional vitelline circulation

cellular
• in contrast to platelets, fibroblasts derived from E12.0 mutant embryos or adult lung fail to exhibit thrombin-induced phopshoinositide hydrolysis and calcium mobilization

growth/size/body
• at E9.0-E9.5, homozygotes display a global developmental delay
• however, those that survive past E9.0-E10.0 catch up with control embryos by E11.5 and develop normally to birth
• starting at E9.0, mutant embryos become uniformly smaller than wild-type embryos

hematopoietic system
N
• surviving homozygotes display normal tail bleeding times and no bleeding diathesis relative to wild-type
• in addition, mutant platelets display strong thrombin-induced responses




Genotype
MGI:3521664
cx5
Allelic
Composition
F2rtm1Ajc/F2rtm1Ajc
F5tm1Dgi/F5tm1Dgi
Genetic
Background
B6.Cg-F5tm1Dgi F2rtm1Ajc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
F2rtm1Ajc mutation (2 available); any F2r mutation (26 available)
F5tm1Dgi mutation (1 available); any F5 mutation (159 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• only 4% of double mutant embryos survive to E12.5
• this rate is significantly lower than that of either F2rtm1Ajc or F5tm1Dgi single mutants (52% or 67% at E12.5, respectively)

cardiovascular system
• double homozygous mutant embryos exhibit pericardial effusions
• double mutant embryos are pale and display bleeding in the exocoelomic cavity
• double mutant embryos exhibit bleeding in the pericardial cavity

embryo
• double homozygous mutant embryos appear runted and necrotic

growth/size/body
• double homozygous mutant embryos appear runted and necrotic

homeostasis/metabolism
• double homozygous mutant embryos exhibit pericardial effusions
• double mutant embryos exhibit bleeding in the pericardial cavity




Genotype
MGI:5440276
cx6
Allelic
Composition
F2rtm1Ajc/F2rtm1Ajc
St14tm1Bug/St14tm1Bug
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
F2rtm1Ajc mutation (2 available); any F2r mutation (26 available)
St14tm1Bug mutation (0 available); any St14 mutation (45 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• expected numbers are found at midgestation

embryo
N
• no neural tube defects are seen




Genotype
MGI:5440277
cx7
Allelic
Composition
F2rtm1Ajc/F2rtm1Ajc
F2rl1tm1Cgh/F2rl1tm1Cgh
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
F2rl1tm1Cgh mutation (3 available); any F2rl1 mutation (60 available)
F2rtm1Ajc mutation (2 available); any F2r mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
embryo
• neural tube defects are largely confined to the hindbrain region with only 5% showing involvement of the midbrain and none showing forebrain involvement
• defects generally only become obvious after E10.5
• occasional

nervous system
• neural tube defects are largely confined to the hindbrain region with only 5% showing involvement of the midbrain and none showing forebrain involvement
• defects generally only become obvious after E10.5
• occasional

limbs/digits/tail
• occasional




Genotype
MGI:3784875
cx8
Allelic
Composition
F2rtm1Ajc/F2rtm1Ajc
F2rl1tm1Cgh/F2rl1tm1Cgh
F2rl3tm1Cgh/F2rl3tm1Cgh
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
F2rl1tm1Cgh mutation (3 available); any F2rl1 mutation (60 available)
F2rl3tm1Cgh mutation (0 available); any F2rl3 mutation (21 available)
F2rtm1Ajc mutation (2 available); any F2r mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging




Genotype
MGI:3784874
cx9
Allelic
Composition
F2rtm1Ajc/F2rtm1Ajc
F2rl1tm1Cgh/F2rl1tm1Cgh
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
F2rl1tm1Cgh mutation (3 available); any F2rl1 mutation (60 available)
F2rtm1Ajc mutation (2 available); any F2r mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• female mice exhibit a decreased survival following exposure to endotoxin compared to wild-type mice
• only 5 % of expected mice are born and survive into adulthood to reproduce
• only 5% of expected mice were born
• however, surviving mice survive into adulthood

immune system
• female mice exhibit a decreased survival following exposure to endotoxin compared to wild-type mice and produce more cytokines at low doses of endotoxin





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