All Phenotypes Fgfr4<tm1Cxd> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Fgfr4^tm1Cxd/Fgfr4^tm1Cxd	involves: 129S6/SvEvTac * Black Swiss	MGI:3653043
cx2	Fgfr3^tm1Led/Fgfr3^tm1Led Fgfr4^tm1Cxd/Fgfr4^tm1Cxd	involves: 129S6/SvEvTac * Black Swiss	MGI:3653045
cx3	Fgfr4^tm1Cxd/Fgfr4^tm1Cxd Tg(Myl2-FGF19)1Dfre/0	involves: 129S6/SvEvTac * FVB/N	MGI:5438226

Allelic Composition	Fgfr4^tm1Cxd/Fgfr4^tm1Cxd
Genetic Background	involves: 129S6/SvEvTac * Black Swiss

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr4^tm1Cxd mutation (0 available); any Fgfr4 mutation (42 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

growth/size/body

decreased body weight ( J:50677 )

• homozygotes are viable, fertile and exhibit no gross phenotypic abnormalities in lung or any other organ, except for a 10% reduction in body weight observed at weaning

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

premature death ( J:50677 )

• double homozygotes usually die within the first few months of life

• no double homozygotes survive beyond ~8 months

respiratory system

impaired lung alveolus development ( J:50677 )

• although morphologically normal at P2, double mutant lungs fail to undergo secondary septation to delineate alveoli at P9 and retain a simplified, immature lung parenchyma architecture with abnormally smooth airway walls at P21

• however, no differences in surfactant protein production, cellular proliferation or apoptosis are observed

absent pulmonary alveoli ( J:50677 )

• double mutant lungs lack identifiable alveoli

emphysema ( J:50677 )

• although outwardly normal, double mutant lungs are histologically emphysematous with a ~3-fold enlargement of the air spaces

abnormal pulmonary elastic fiber morphology ( J:50677 )

• starting at ~P21 (i.e. after alveogenesis), double mutant lungs exhibit significantly increased levels of elastin deposition relative to control lungs

• however, no differences in elastin deposition or elastin fiber morphology are observed before or during alveogenesis

growth/size/body

decreased body size ( J:50677 )

• at weaning, double homozygotes are ~50% the size of control siblings, despite an apparently normal birth size

postnatal growth retardation ( J:50677 )

• double homozygotes exhibit significant postnatal growth retardation relative to control siblings

reproductive system

infertility ( J:50677 )

• double homozygotes are largely infertile, although a few are able to produce progeny

homeostasis/metabolism

dehydration ( J:50677 )

• double homozygotes appear sickly and dehydrated

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
lower respiratory tract disease		DOID:0050161		J:50677

Allelic Composition	Fgfr4^tm1Cxd/Fgfr4^tm1Cxd Tg(Myl2-FGF19)1Dfre/0
Genetic Background	involves: 129S6/SvEvTac * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr4^tm1Cxd mutation (0 available); any Fgfr4 mutation (42 available)
Tg(Myl2-FGF19)1Dfre mutation (0 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

decreased incidence of tumors by chemical induction ( J:187236 )

• the hepatocarcinogenesis observed in diethylnitrosamine (DEN) treated single Tg(Myl2-FGF19)1Dfre mutants is abolished in double mutants

decreased liver tumor incidence ( J:187236 )

• mutants do not develop gross or histological evidence of hepatocellular neoplasia unlike single Tg(Myl2-FGF19)1Dfre mutant mice which develop hepatocellular carcinoma

• the preneoplastic hepatocellular proliferation that is seen in single Tg(Myl2-FGF19)1Dfre mutants is not evident in double mutants