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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Fgfr1tm1Upir
targeted mutation 1, Ulla Pirvola
MGI:3528437
Summary 11 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Fgfr1tm1Upir/Fgfr1tm1.1Upir involves: C57BL/6J MGI:3529288
cn2
Cpa3tm3(icre)Hrr/Cpa3+
Fgfr1tm1Upir/Fgfr1tm1Upir
Fgfr2tm1Dor/Fgfr2tm1Dor
Tg(KRT5-cre)5132Jlj/0
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * C57BL/6J * DBA/2J MGI:5642134
cn3
Fgfr1tm1Upir/Fgfr1tm1Upir
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * ICR MGI:3702999
cn4
Fgfr1tm1Upir/Fgfr1tm1.1Upir
Foxg1tm1(cre)Skm/Foxg1+
involves: 129P2/OlaHsd * ICR MGI:3702998
cn5
Fgfr1tm1Upir/Fgfr1tm1Upir
Fgfr2tm1Dor/Fgfr2tm1Dor
Gt(ROSA)26Sortm1(Cdkn1b,EGFP)Dor/Gt(ROSA)26Sor+
Myl2tm1(cre)Krc/Myl2+
involves: 129/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 MGI:3775280
cn6
Fgfr1tm1Upir/Fgfr1tm1Upir
Fgfr2tm1Dor/Fgfr2tm1Dor
Tg(KRT5-cre)5132Jlj/0
involves: 129X1/SvJ * C57BL/6 * C57BL/6J * DBA/2J MGI:5642117
cn7
Fgfr1tm1Upir/Fgfr1tm1Upir
Fgfr2tm1Dor/Fgfr2tm1Dor
Tg(GFAP-cre)25Mes/0
involves: 129X1/SvJ * FVB/N MGI:3641106
cn8
Fgfr1tm1Upir/Fgfr1tm1Upir
Tg(KRT5-cre)5132Jlj/0
involves: C57BL/6 * C57BL/6J * DBA/2J MGI:5642114
cn9
Fgfr1tm1Upir/Fgfr1tm1Upir
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:3641104
cn10
Fgfr1tm1Upir/Fgfr1tm1Upir
Tg(GFAP-cre)25Mes/0
involves: FVB/N MGI:3641103
cn11
Fgfr1tm1Upir/Fgfr1tm1Upir
Tg(Mnx1-GFP)1Slp/?
Tg(Nes-cre)1Kln/?
Not Specified MGI:3767836


Genotype
MGI:3529288
cn1
Allelic
Composition
Fgfr1tm1Upir/Fgfr1tm1.1Upir
Genetic
Background
involves: C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr1tm1.1Upir mutation (0 available); any Fgfr1 mutation (172 available)
Fgfr1tm1Upir mutation (0 available); any Fgfr1 mutation (172 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• the thickness of each band of cardiac actin is increased and average sarcomere thickness is increased to 1.01 um compared to 0.65 um in wild-type
• at E12.5 the ventricular wall is thinner than normal
• individual cardiomyoblasts appear larger and premature differentiation of cardiomyoblasts is seen
• at E12.5 the atria are enlarged
• severe hypoplasia is seen, however the patterning of the cardiac cushions, septum, and ventricular layers appears normal
• at E12.5 the heart does not fill the pericardial space
• hypoplasia is more severe and uniform than in Fgf9tm1Dor homozygotes
• biventricular dilation is seen in newborn mutants
• biventricular dilation is seen in newborn mutants
• myocardial proliferation is decreased throughout the base and apex of both ventricles

muscle
• the thickness of each band of cardiac actin is increased and average sarcomere thickness is increased to 1.01 um compared to 0.65 um in wild-type
• at E12.5 the ventricular wall is thinner than normal
• myocardial proliferation is decreased throughout the base and apex of both ventricles

cellular
• myocardial proliferation is decreased throughout the base and apex of both ventricles




Genotype
MGI:5642134
cn2
Allelic
Composition
Cpa3tm3(icre)Hrr/Cpa3+
Fgfr1tm1Upir/Fgfr1tm1Upir
Fgfr2tm1Dor/Fgfr2tm1Dor
Tg(KRT5-cre)5132Jlj/0
Genetic
Background
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * C57BL/6J * DBA/2J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cpa3tm3(icre)Hrr mutation (0 available); any Cpa3 mutation (22 available)
Fgfr1tm1Upir mutation (0 available); any Fgfr1 mutation (172 available)
Fgfr2tm1Dor mutation (2 available); any Fgfr2 mutation (23 available)
Tg(KRT5-cre)5132Jlj mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body

integument
• increase in transepidermal water loss, indicating an epidermal barrier defect

hematopoietic system

homeostasis/metabolism
• increase in transepidermal water loss, indicating an epidermal barrier defect

immune system

cellular

reproductive system
• all females are sterile
• most males are sterile




Genotype
MGI:3702999
cn3
Allelic
Composition
Fgfr1tm1Upir/Fgfr1tm1Upir
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * ICR
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr1tm1Upir mutation (0 available); any Fgfr1 mutation (172 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• phenotype is stated to be comparable to that of mice that are compound heterozygous for Fgfr1tm1.1Upir and Fgfr1tm1Upir and also heterozygous for Foxg1tm1(cre)Skm; however, no data are presented in J:78879

hearing/vestibular/ear




Genotype
MGI:3702998
cn4
Allelic
Composition
Fgfr1tm1Upir/Fgfr1tm1.1Upir
Foxg1tm1(cre)Skm/Foxg1+
Genetic
Background
involves: 129P2/OlaHsd * ICR
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr1tm1.1Upir mutation (0 available); any Fgfr1 mutation (172 available)
Fgfr1tm1Upir mutation (0 available); any Fgfr1 mutation (172 available)
Foxg1tm1(cre)Skm mutation (2 available); any Foxg1 mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants die within 24 hrs after birth

hearing/vestibular/ear
• at birth, mutant cochleae are frequently slightly shorter than normal
• however, mutant otocysts appear morphologically normal at E10.5 and E11.5
• in addition, initiation of cochlear duct outgrowth from the otocyst is unaffected at E12.5
• at birth, the sensory epithelium of the upper cochlear half is arranged in small sensory patches that mainly consist of IHCs and pillar supporting cells, while the lower cochlear half is less severely affected
• in contrast, the vestibular sensory epithelium remains unchanged
• at around birth, the organ of Corti is severely disrupted due to impaired production of precursor cells between E12 and E15, as shown by BrdU labeling
• at E16.5, mutants display no molecular signs of HC specification or differentiation in the gap regions found between sensory patches; OHCs are more severely affected
• at E16.5, the remaining HCs in the sensory patches appear to undergo normal differentiation
• at E18.5, most cochlear sections are devoid of HCs and the greater epithelial ridge is abnormally thin, due to reduced precursor cell proliferation in the ventral wall of the cochlear duct between E12 and E15.5
• apparently, the remaining precursors of the organ of Corti preferentially differentiate into IHCs and pillar cells
• no differences in precursor cell proliferation rate are observed in the dorsal, non-sensory wall of the cochlear duct
• at P0, mutants show a 85% reduction in the total number of differentiating HCs relative to wild-type mice
• at birth, only very low numbers of OHCs are formed, and these are located in lower cochlear half
• at birth, the small sensory patches found in the upper cochlear half frequently show doublet IHCs instead of a single continuous IHC row
• at birth, the small sensory patches found in the upper cochlear half frequently show an accumulation of disorientated IHCs at the edges
• at birth, the sensory patches found in the upper cochlear half frequently show no signs of differentiation of supporting cells

nervous system
• at E16.5, mutants display no molecular signs of HC specification or differentiation in the gap regions found between sensory patches; OHCs are more severely affected
• at E16.5, the remaining HCs in the sensory patches appear to undergo normal differentiation
• at E18.5, most cochlear sections are devoid of HCs and the greater epithelial ridge is abnormally thin, due to reduced precursor cell proliferation in the ventral wall of the cochlear duct between E12 and E15.5
• apparently, the remaining precursors of the organ of Corti preferentially differentiate into IHCs and pillar cells
• no differences in precursor cell proliferation rate are observed in the dorsal, non-sensory wall of the cochlear duct
• at P0, mutants show a 85% reduction in the total number of differentiating HCs relative to wild-type mice
• at birth, only very low numbers of OHCs are formed, and these are located in lower cochlear half
• at birth, the small sensory patches found in the upper cochlear half frequently show doublet IHCs instead of a single continuous IHC row
• at birth, the small sensory patches found in the upper cochlear half frequently show an accumulation of disorientated IHCs at the edges




Genotype
MGI:3775280
cn5
Allelic
Composition
Fgfr1tm1Upir/Fgfr1tm1Upir
Fgfr2tm1Dor/Fgfr2tm1Dor
Gt(ROSA)26Sortm1(Cdkn1b,EGFP)Dor/Gt(ROSA)26Sor+
Myl2tm1(cre)Krc/Myl2+
Genetic
Background
involves: 129/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr1tm1Upir mutation (0 available); any Fgfr1 mutation (172 available)
Fgfr2tm1Dor mutation (2 available); any Fgfr2 mutation (23 available)
Gt(ROSA)26Sortm1(Cdkn1b,EGFP)Dor mutation (0 available); any Gt(ROSA)26Sor mutation (502 available)
Myl2tm1(cre)Krc mutation (2 available); any Myl2 mutation (11 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mice exhibit smaller hearts than mice homozygous for null alleles of Fgfr1 and Fgfr2 due to decreased myocardial proliferation
• however, coronary development is normal
• mice exhibit thinner ventricular walls than mice homozygous for null alleles of Fgfr1 and Fgfr2




Genotype
MGI:5642117
cn6
Allelic
Composition
Fgfr1tm1Upir/Fgfr1tm1Upir
Fgfr2tm1Dor/Fgfr2tm1Dor
Tg(KRT5-cre)5132Jlj/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6 * C57BL/6J * DBA/2J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr1tm1Upir mutation (0 available); any Fgfr1 mutation (172 available)
Fgfr2tm1Dor mutation (2 available); any Fgfr2 mutation (23 available)
Tg(KRT5-cre)5132Jlj mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body

integument
• keratinocyte proliferation is mildly increased at P18 and is strongly increased in the back and tail skin at 3 months of age (J:158802)
• however, keratinocytes in vitro show normal proliferation rate (J:158802)
• transepidermal water loss is slightly increased at P18 and is significantly increased at 6 months of age, indicating disturbed epidermal barrier function (J:158802)
• progressive skin inflammation, with a 60% increase in epidermal gamma-delta T cells, an increase in mast cells in the dermis, and increase in CD45+ alpha-beta and gamma-delta T cells in the dermis (J:158802)
• however, macrophage or neutrophil infiltrate is not seen (J:158802)
• loss of skin appendages
• sebaceous glands are virtually absent in the back skin of older mice
• mice are hairless by 2-4 months of age
• progressive hair loss and mice are hairless by 2-4 months of age (J:158802)
• hair follicles are abnormally shaped at P18 (first telogen)
• hair follicles are virtually absent in the back skin of older mice and only a few cysts are present in the dermis
• hair follicles are smaller at P18 (first telogen), but numbers are normal
• by P30, most follicles are in telogen compared to controls which have entered the second anagen
• a mild hypotrophy of the epidermis is seen at P5 (first anagen), but the dermis and appendages appear normal
• mice show only a rudimentary development of tight junctions in the epidermis
• bubble-like intercellular clefts between the keratinocytes of the stratum granulosum
• mice develop epidermal hyperthickening combined with disorganization of the keratinocytes at 2-3 months of age which progresses with age (J:158802)
• fragile appearing skin
• fibrosis develops in the dermis

endocrine/exocrine glands
• sebaceous glands are virtually absent in the back skin of older mice

cellular
• keratinocyte proliferation is mildly increased at P18 and is strongly increased in the back and tail skin at 3 months of age (J:158802)
• however, keratinocytes in vitro show normal proliferation rate (J:158802)

hematopoietic system
• mast cells in young cells are degranulated, followed by a decrease in degranulated mast cells thereafter
• increase in mast cell number between P7 and P9 is greater in mutants than in controls and remains high unlike in controls which show a decrease over time
• higher number of mast cell progenitors in the white adipose tissue
• mice show enhanced levels of IgE in the dermis and in the serum
• mice show enhanced levels of IgG1 in the dermis
• mice show enhanced levels of IgG2a in the dermis

homeostasis/metabolism
• transepidermal water loss is slightly increased at P18 and is significantly increased at 6 months of age, indicating disturbed epidermal barrier function (J:158802)
• transient increase in mast cell chemokines in the epidermis and dermis

immune system
• mast cells in young cells are degranulated, followed by a decrease in degranulated mast cells thereafter
• increase in mast cell number between P7 and P9 is greater in mutants than in controls and remains high unlike in controls which show a decrease over time
• higher number of mast cell progenitors in the white adipose tissue
• mice show enhanced levels of IgE in the dermis and in the serum
• mice show enhanced levels of IgG1 in the dermis
• mice show enhanced levels of IgG2a in the dermis
• transient increase in mast cell chemokines in the epidermis and dermis
• progressive skin inflammation, with a 60% increase in epidermal gamma-delta T cells, an increase in mast cells in the dermis, and increase in CD45+ alpha-beta and gamma-delta T cells in the dermis (J:158802)
• however, macrophage or neutrophil infiltrate is not seen (J:158802)

behavior/neurological
• high consumption of drinking water

reproductive system
• all females are infertile (J:158802)
• about 60% of males are infertile (J:158802)

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
atopic dermatitis DOID:3310 OMIM:603165
OMIM:PS603165
J:221184




Genotype
MGI:3641106
cn7
Allelic
Composition
Fgfr1tm1Upir/Fgfr1tm1Upir
Fgfr2tm1Dor/Fgfr2tm1Dor
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr1tm1Upir mutation (0 available); any Fgfr1 mutation (172 available)
Fgfr2tm1Dor mutation (2 available); any Fgfr2 mutation (23 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• numbers of astrocytes reaching the cortex is significantly reduced compared to controls at P7




Genotype
MGI:5642114
cn8
Allelic
Composition
Fgfr1tm1Upir/Fgfr1tm1Upir
Tg(KRT5-cre)5132Jlj/0
Genetic
Background
involves: C57BL/6 * C57BL/6J * DBA/2J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr1tm1Upir mutation (0 available); any Fgfr1 mutation (172 available)
Tg(KRT5-cre)5132Jlj mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• no obvious abnormalities are seen at any stage of postnatal development




Genotype
MGI:3641104
cn9
Allelic
Composition
Fgfr1tm1Upir/Fgfr1tm1Upir
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr1tm1Upir mutation (0 available); any Fgfr1 mutation (172 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• mice have defects in the dorsal telencephalic commissures
• all mutants have a complete absence of midline crossing at the most anterior and posterior region
• about 20% of mice have a small number of callosal fibers in the region above the hippocampal commissure
• axons are absent in the contralateral cortex or white matter
• the cortical fibers are trapped within Probst bundles




Genotype
MGI:3641103
cn10
Allelic
Composition
Fgfr1tm1Upir/Fgfr1tm1Upir
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr1tm1Upir mutation (0 available); any Fgfr1 mutation (172 available)
Tg(GFAP-cre)25Mes mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• in mutants, midline cells do not migrate from the ventricular zone to the subpial region of the dorsomedial pallium
• average midline width of the dorsal commissures is markedly smaller compared to controls; anterior and posterior are significantly more affected than the middle
• in 83% of mice, there is a complete loss of callosal axons from the motor and somatosensory cortex at birth
• there is a loss of hippocampal commissural axons in neonatal mice
• idusium griseum astroglia are absent in the anterior regions of mutants
• processes emerging from the glial wedge and ventricular zone remain attached at the ventricular zone and the pia and very few astrocytes are observed in between the glial wedge and the idusium griseum
• numbers of astrocytes reaching the cortex are significantly reduced compared to controls

cellular
• in mutants, midline cells do not migrate from the ventricular zone to the subpial region of the dorsomedial pallium




Genotype
MGI:3767836
cn11
Allelic
Composition
Fgfr1tm1Upir/Fgfr1tm1Upir
Tg(Mnx1-GFP)1Slp/?
Tg(Nes-cre)1Kln/?
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr1tm1Upir mutation (0 available); any Fgfr1 mutation (172 available)
Tg(Mnx1-GFP)1Slp mutation (0 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• mice display motor axon guidance defects in the area where medial-class spinal motor neuron axons turn from the spinal nerve towards the dermomyotome
• mice display motor axon guidance defects in the area where medial-class spinal motor neuron axons turn from the spinal nerve towards the dermomyotome
• motor neuron axons are less fasciculated than in heterozygotes
• unlike in wild-type mice, motor neuron axons growth far into the dorsal root ganglia

cellular
• mice display motor axon guidance defects in the area where medial-class spinal motor neuron axons turn from the spinal nerve towards the dermomyotome





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last database update
10/15/2019
MGI 6.14
The Jackson Laboratory