All Phenotypes Fgf15<tm1Sms> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Fgf15^tm1Sms/Fgf15^tm1Sms	involves: 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:3045809
ht2	Fgf15^tm1Sms/Fgf15⁺	involves: 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:3639489
cn3	Fgf15^tm1Sms/Fgf15^tm1Sms Gt(ROSA)26Sor^tm1Sor/Gt(ROSA)26Sor⁺ H2az2^{Tg(Wnt1-cre)11Rth}/H2az2⁺	involves: 129S1/Sv * 129S4/SvJaeSor * 129X1/SvJ * C57BL/6 * CBA	MGI:3639491
cx4	Fgf15^tm1Sms/Fgf15⁺ Tbx1^tm1Bld/Tbx1⁺	involves: 129S1/Sv * 129S7/SvEvBrd * 129X1/SvJ * C57BL/6	MGI:3639490

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

Fgf15^tm1Sms/Fgf15^tm1Sms mice display cardiovascular defects

mortality/aging

lethality throughout fetal growth and development, incomplete penetrance ( J:97317 )

• on a predominantly C57BL/6 genetic background, homozygotes are obtained at a slightly reduced Mendelian frequency between E13.5 and E18.5 (16.37% vs expected 25%)

postnatal lethality ( J:97317 )

• on a predominantly C57BL/6 genetic background, a significant number of homozygotes die between P0 and P7

• only about 3% of homozygotes are recovered by P21

cardiovascular system

abnormal aorta morphology ( J:97317 )

• at E18.5, 63.2% of homozygotes exhibit failure of the aorta to wedge between the mitral and tricuspid atrioventricular valves

aberrant origin of the right subclavian artery ( J:97317 )

• at E18.5, aberrant origin of the right subclavian artery is noted in 11.1% of homozygotes

abnormal cardiac outflow tract development ( J:97317 )

• at E18.5, most homozygotes show abnormal cardiac outflow tract alignment, such as abnormal positioning of the aorta relative to the pulmonary trunk and AV valves; however, the behavior of secondary heart field cells appears unaffected

• at E18.5, only 1 of 19 mutant hearts appears grossly normal, consistent with a small number of viable "escapers"

• notably, at E10.5 (but not earlier) homozygotes show a small but significant reduction in cell proliferation in the outflow tract myocardium, in the absence of abnormal apoptosis

double outlet right ventricle ( J:97317 )

• at E18.5, 26.3% of homozygotes display double outlet right ventricle

overriding aortic valve ( J:97317 )

• at E18.5, 21.1% of homozygotes display an overriding aorta

atrial septal defect ( J:97317 )

• at E18.5, 5.26% of homozygotes display an atrial septal defect

atrioventricular septal defect ( J:97317 )

• at E18.5, 5.26% of homozygotes display an atrioventricular canal defect

abnormal interventricular septum morphology ( J:97317 )

• at E18.5, most homozygotes show abnormal interventricular septation

ventricular septal defect ( J:97317 )

• at E18.5, ~90% of homozygotes show either a membranous ventricular septal defect (VSD), a muscular VSD, in which the septal defect traverses the muscular wall of the septum, or both

perimembraneous ventricular septal defect ( J:97317 )

muscular ventricular septal defect ( J:97317 )

hearing/vestibular/ear

hearing/vestibular/ear phenotype ( J:90407 )

N	• surviving homozygotes exhibit normal balance and auditory brainstem responses • in addition, homozygotes display normal otic induction and otic vesicle formation at E9.5-E10.5

Allelic Composition	Fgf15^tm1Sms/Fgf15⁺
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgf15^tm1Sms mutation (1 available); any Fgf15 mutation (15 available)

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

mortality/aging

postnatal lethality ( J:97317 )

• on a predominantly C57BL/6 genetic background, heterozygotes are obtained at a slightly reduced Mendelian frequency between P0 and P7 (44.44% vs expected 50%)

cardiovascular system

overriding aortic valve ( J:97317 )

• at E18.5, 9.1% of heterozygotes display an overriding aorta; however, no aortic arch patterning defects are observed

ventricular septal defect ( J:97317 )

• at E18.5, 18.2% of heterozygotes exhibit muscular and membranous ventricular septal defects

perimembraneous ventricular septal defect ( J:97317 )

muscular ventricular septal defect ( J:97317 )

Allelic Composition	Fgf15^tm1Sms/Fgf15^tm1Sms Gt(ROSA)26Sor^tm1Sor/Gt(ROSA)26Sor⁺ H2az2^{Tg(Wnt1-cre)11Rth}/H2az2⁺
Genetic Background	involves: 129S1/Sv * 129S4/SvJaeSor * 129X1/SvJ * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgf15^tm1Sms mutation (1 available); any Fgf15 mutation (15 available)
Gt(ROSA)26Sor^tm1Sor mutation (7 available); any Gt(ROSA)26Sor mutation (993 available)
H2az2^{Tg(Wnt1-cre)11Rth} mutation (2 available); any H2az2 mutation (26 available)

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

embryo

decreased cardiac neural crest cell number ( J:97317 )

• at E12.5, homozygotes exhibit successful septation of the distal outflow tract; however, the number of NCCs contributing to the proximal outflow tract is significantly reduced

abnormal cardiac neural crest cell migration ( J:97317 )

• at E9.5, cardiac NCCs migrate to the developing caudal pharyngeal arches of mutant embryos in numbers comparable to those of wild-type embryos; however, at E11.5, NCCs fail to invaginate on the right side of the proximal aortic sac at the level of its connection with the 6th aortic arch arteries

• as a result, the conotruncal cushions remain oriented laterally relative to one another

cardiovascular system

decreased cardiac neural crest cell number ( J:97317 )

• at E12.5, homozygotes exhibit successful septation of the distal outflow tract; however, the number of NCCs contributing to the proximal outflow tract is significantly reduced

abnormal cardiac outflow tract development ( J:97317 )

• homozygotes exhibit abnormal NCC behavior during outflow tract remodeling

nervous system

decreased cardiac neural crest cell number ( J:97317 )

• at E12.5, homozygotes exhibit successful septation of the distal outflow tract; however, the number of NCCs contributing to the proximal outflow tract is significantly reduced

cellular

abnormal cardiac neural crest cell migration ( J:97317 )

• as a result, the conotruncal cushions remain oriented laterally relative to one another

Allelic Composition	Fgf15^tm1Sms/Fgf15⁺ Tbx1^tm1Bld/Tbx1⁺
Genetic Background	involves: 129S1/Sv * 129S7/SvEvBrd * 129X1/SvJ * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgf15^tm1Sms mutation (1 available); any Fgf15 mutation (15 available)
Tbx1^tm1Bld mutation (1 available); any Tbx1 mutation (36 available)

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

cardiovascular system

abnormal aortic arch development ( J:97317 )

• at E18.5, double heterozygotes show no significant increase in the penetrance or severity of aortic arch patterning defects relative to Tbx1^tm1Bld heterozygotes

• observed defects include interrupted aortic arch type-B (20%), aberrant origin of the right subclavian artery (30%), and VSDs (membranous 20%; muscular: 10%)

aberrant origin of the right subclavian artery ( J:97317 )

interrupted aortic arch ( J:97317 )

perimembraneous ventricular septal defect ( J:97317 )

muscular ventricular septal defect ( J:97317 )

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)
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