All Phenotypes Adam9<tm1Bbl> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Adam9^tm1Bbl/Adam9^tm1Bbl	involves: 129	MGI:4360909
cx2	Adam12^tm1Asf/Adam12^tm1Asf Adam15^tm1Bbl/Adam15^tm1Bbl Adam19^{Gt(Betageo)1Bbl}/Adam19^{Gt(Betageo)1Bbl} Adam9^tm1Bbl/Adam9^tm1Bbl	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:3654840
cx3	Adam12^tm1Asf/Adam12^tm1Asf Adam15^tm1Bbl/Adam15^tm1Bbl Adam17^tm1Imx/Adam17^tm1Imx Adam9^tm1Bbl/Adam9^tm1Bbl	involves: 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:3056935
cx4	Adam19^{Gt(Betageo)1Bbl}/Adam19^{Gt(Betageo)1Bbl} Adam9^tm1Bbl/Adam9^tm1Bbl	involves: 129/Sv * 129P2/OlaHsd * C57BL/6	MGI:3654838

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

cellular

increased keratinocyte migration ( J:161698 )

• increased migration rate to mutant wound sites

homeostasis/metabolism

enhanced wound healing ( J:161698 )

• mutant mice show accelerated wound repair compared with controls

• re-epithelialization was significantly faster in mutant wounds than control wounds

integument

increased keratinocyte migration ( J:161698 )

• increased migration rate to mutant wound sites

neoplasm

decreased tumor growth/size ( J:148993 )

• tumor growth from heterotopically injected B16F0 melanoma cells was reduced in mutant mice

cardiovascular system

abnormal induced retina neovascularization ( J:148993 )

• pathological neovascularization in both oxygen-induced retinopathy (OIR) and laser-induced choroidal neovascularization (CNV) models is significantly reduced in mutant retinas

pigmentation

abnormal retina pigment epithelium morphology ( J:150865 )

• at 12 months, mutant retinas show extended malformed, vesiculated retinal pigment epithelial cell apical processes and disrupted contact with the photoreceptor outer segment

• at 20 months, mutant retinas show unusual infoldings of the basal membrane of the retinal pigment epithelium

normal phenotype

no abnormal phenotype detected ( J:74655 )

• mutant mice are viable and fertile, with normal pathology, histology and behavior noted up to two years of age

vision/eye

abnormal induced retina neovascularization ( J:148993 )

• pathological neovascularization in both oxygen-induced retinopathy (OIR) and laser-induced choroidal neovascularization (CNV) models is significantly reduced in mutant retinas

abnormal retina layer morphology ( J:150865 )

• histological analysis of 12 month old mutant mice showed an abnormal gap between the photoreceptor outer segment and the retinal pigment epithelium

• mutant retinas show extended malformed, vesiculated retinal pigment epithelial cell apical processes and disrupted contact with the photoreceptor outer segment

• at 20 months, mutants show a disorganized photoreceptor outer segment and a thinning outer nuclear layer, macrophages within the gap between the photoreceptor outer segment and the retinal pigment epithelium, and material could also be seen deposited between the RPE and Bruchs membrane

abnormal retina pigment epithelium morphology ( J:150865 )

• at 12 months, mutant retinas show extended malformed, vesiculated retinal pigment epithelial cell apical processes and disrupted contact with the photoreceptor outer segment

• at 20 months, mutant retinas show unusual infoldings of the basal membrane of the retinal pigment epithelium

abnormal retina neuronal layer morphology ( J:150865 )

increased susceptibility to age-related retinal degeneration ( J:150865 )

• progressive with age

decreased a-wave amplitude ( J:150865 )

• at 12 months of age, mutants show a saturated response of approximately 50% the amplitude of wild-type mice

• at 20 months of age, mutants show a saturated a-wave responses approximately 30% the amplitude of the age-matched wild-type

decreased b-wave amplitude ( J:150865 )

• at 12 months of age, mutants show a saturated b-wave response approximately 30% the amplitude of the age-matched wild-type

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
cone-rod dystrophy 9		DOID:0111020	OMIM:612775	J:150865

Allelic Composition	Adam12^tm1Asf/Adam12^tm1Asf Adam15^tm1Bbl/Adam15^tm1Bbl Adam19^{Gt(Betageo)1Bbl}/Adam19^{Gt(Betageo)1Bbl} Adam9^tm1Bbl/Adam9^tm1Bbl
Genetic Background	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adam12^tm1Asf mutation (0 available); any Adam12 mutation (42 available)
Adam15^tm1Bbl mutation (0 available); any Adam15 mutation (37 available)
Adam19^{Gt(Betageo)1Bbl} mutation (1 available); any Adam19 mutation (78 available)
Adam9^tm1Bbl mutation (1 available); any Adam9 mutation (45 available)

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

mortality/aging

perinatal lethality, incomplete penetrance ( J:99649 )

• significantly less (4.6%) than the expected Mendelian ratio of 25% of mutants is seen at birth, however normal numbers are seen at E18.5 although less than 1/3 have a visible heartbeat at this time

cardiovascular system

double outlet right ventricle ( J:99649 )

• both the aorta and pulmonic artery emanate from the right ventricle, a more severe malrotation defect than seen in single homozygous Adam19 mutant mice

ventricular septal defect ( J:99649 )

• exhibit a ventricular septal defect at E18.5

abnormal heart valve morphology ( J:99649 )

abnormal mitral valve morphology ( J:99649 )

• thicker and misshapen mitral valve

thick mitral valve ( J:99649 )

abnormal tricuspid valve morphology ( J:99649 )

• misshapen tricuspid valve

tricuspid valve hyperplasia ( J:99649 )

• hyperplastic tricuspid valve

semilunar valve hyperplasia ( J:99649 )

• hyperplastic semilunar valves

Allelic Composition	Adam12^tm1Asf/Adam12^tm1Asf Adam15^tm1Bbl/Adam15^tm1Bbl Adam17^tm1Imx/Adam17^tm1Imx Adam9^tm1Bbl/Adam9^tm1Bbl
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adam12^tm1Asf mutation (0 available); any Adam12 mutation (42 available)
Adam15^tm1Bbl mutation (0 available); any Adam15 mutation (37 available)
Adam17^tm1Imx mutation (0 available); any Adam17 mutation (64 available)
Adam9^tm1Bbl mutation (1 available); any Adam9 mutation (45 available)

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

mortality/aging

neonatal lethality ( J:88801 )

cardiovascular system

abnormal mitral valve morphology ( J:88801 )

• thickened and misshapen valves

thick mitral valve ( J:88801 )

abnormal tricuspid valve morphology ( J:88801 )

• thickened and misshapen valves

thick tricuspid valve ( J:88801 )

abnormal aortic valve morphology ( J:88801 )

• thickened and misshapen valves

thick aortic valve ( J:88801 )

abnormal pulmonary valve morphology ( J:88801 )

• thickened and misshapen valves

thick pulmonary valve ( J:88801 )

vision/eye

eyelids open at birth ( J:88801 )

Allelic Composition	Adam19^{Gt(Betageo)1Bbl}/Adam19^{Gt(Betageo)1Bbl} Adam9^tm1Bbl/Adam9^tm1Bbl
Genetic Background	involves: 129/Sv * 129P2/OlaHsd * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adam19^{Gt(Betageo)1Bbl} mutation (1 available); any Adam19 mutation (78 available)
Adam9^tm1Bbl mutation (1 available); any Adam9 mutation (45 available)

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

cardiovascular system

double outlet right ventricle ( J:99649 )

abnormal mitral valve morphology ( J:99649 )

• misshapen mitral valves at E18.5

enlarged mitral valve ( J:99649 )

• enlarged/thickened mitral valves at E18.5

thick mitral valve ( J:99649 )

• enlarged/thickened mitral valves at E18.5

abnormal tricuspid valve morphology ( J:99649 )

• misshapen tricuspid valve, similar to that seen in single homozygous Adam 19 mutants

thick tricuspid valve ( J:99649 )

• thicker tricuspid valve, similar to that seen in single homozygous Adam 19 mutants

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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