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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Isl1tm1(cre)Sev
targeted mutation 1, Sylvia Evans
MGI:3623159
Summary 18 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Bmp4tm4Blh/Bmp4tm4Blh
Isl1tm1(cre)Sev/Isl1+
involves: 129 * 129S6/SvEvTac MGI:5642272
cn2
Rspo3tm1Arte/Rspo3tm1Arte
Isl1tm1(cre)Sev/Isl1+
involves: 129 * C57BL/6 MGI:5643693
cn3
Nkx2-5tm1Krc/Nkx2-5tm1Krc
Isl1tm1(cre)Sev/Isl1+
involves: 129 * C57BL/6 MGI:5643691
cn4
Isl1tm1(cre)Sev/Isl1+
Pax9tm1Rbal/Pax9tm1.1Hpt
involves: 129 * C57BL/6J MGI:7294563
cn5
Isl1tm1(cre)Sev/Isl1+
Msx1tm1Rilm/Msx1+
Pax9tm1Rbal/Pax9tm1.1Hpt
involves: 129 * CD-1 MGI:7294564
cn6
Juntm4Wag/Juntm4Wag
Isl1tm1(cre)Sev/Isl1+
involves: 129P2/OlaHsd * 129S/Sv MGI:7562242
cn7
Juntm1Pa/Juntm4Wag
Isl1tm1(cre)Sev/Isl1+
involves: 129P2/OlaHsd * 129S/Sv * 129X1/SvJ * C57BL/6J MGI:7562004
cn8
Bcortm1.1Vjba/Y
Isl1tm1(cre)Sev/Isl1+
involves: 129S1/Sv MGI:7343918
cn9
Bcortm1.1Vjba/Bcor+
Isl1tm1(cre)Sev/Isl1+
involves: 129S1/Sv MGI:7343919
cn10
Bmpr1atm2.1Bhr/Bmpr1atm2.2Bhr
Isl1tm1(cre)Sev/Isl1+
involves: 129S4/SvJae * 129S7/SvEvBrd MGI:3625139
cn11
Dvl3tm1Awb/Dvl3tm1Awb
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Isl1tm1(cre)Sev/Isl1+
involves: 129S4/SvJaeSor * 129S6/SvEvTac * Black Swiss MGI:3831923
cn12
Isl1tm1(cre)Sev/Isl1+
Tg(CAG-lacZ,-BMPR1A*,-EGFP)1Mis/0
involves: 129S7/SvEvBrd MGI:5444492
cn13
Irx3tm3Hui/Irx3tm3Hui
Irx5tm3Hui/Irx5tm3Hui
Isl1tm1(cre)Sev/Isl1+
involves: 129S/Sv MGI:5444491
cn14
Fgf8tm2Moon/Fgf8tm1Mrc
Isl1tm1(cre)Sev/Isl1+
involves: 129S/Sv MGI:3639731
cn15
Smotm1Amc/Smotm2Amc
Isl1tm1(cre)Sev/Isl1+
involves: 129S/Sv * 129X1/SvJ MGI:3689403
cn16
Fgf8tm1Mrc/Fgf8tm2Moon
Isl1tm1(cre)Sev/Isl1+
involves: 129S/Sv * Black Swiss * C57BL/6 MGI:3829040
cn17
Epha4tm1.1Bzh/Epha4tm1.1Bzh
Isl1tm1(cre)Sev/Isl1+
Tg(Hlxb9-GFP)1Tmj/0
involves: 129S/Sv * Black Swiss * C57BL/6J * CD-1 * FVB/N MGI:6406420
cn18
Isl1tm1(cre)Sev/Isl1+
Juntm4Wag/Jun+
Not Specified MGI:7562245


Genotype
MGI:5642272
cn1
Allelic
Composition
Bmp4tm4Blh/Bmp4tm4Blh
Isl1tm1(cre)Sev/Isl1+
Genetic
Background
involves: 129 * 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bmp4tm4Blh mutation (0 available); any Bmp4 mutation (21 available)
Isl1tm1(cre)Sev mutation (1 available); any Isl1 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Hindlimb fusion of Bmp4tm4Blh/Bmp4tm4Blh Isl1tm1(cre)Sev/Isl1+ mice

embryo
• hindlimb fusion similar to sirenomelia
• 59% and 36% of mutants have defects consistent with type III (loss of the fibula) and type I (abnormal medial location of fibula), with the other 5% having type V sirenomelia (loss of the fibula and fusion of the femur)
• marker analysis indicates abnormal anterior peri-cloacal mesenchyme formation resulting in hypoplastic anterior peri-cloacal mesenchyme
• the location of hindlimb bud is closely apposed to one another
• marker analysis suggests that posterior hindlimb buds are fused and that early hindlimb bud grows out normally but the midline tissue is missing
• however, the proximal-distal axis of the hindlimb bud is maintained

digestive/alimentary system

limbs/digits/tail
• defective fibula formation, with fibula aberrantly located medially or absent
• defective hindlimb initiation
• hindlimb fusion similar to sirenomelia
• 59% and 36% of mutants have defects consistent with type III (loss of the fibula) and type I (abnormal medial location of fibula), with the other 5% having type V sirenomelia (loss of the fibula and fusion of the femur)
• the location of hindlimb bud is closely apposed to one another
• marker analysis suggests that posterior hindlimb buds are fused and that early hindlimb bud grows out normally but the midline tissue is missing
• however, the proximal-distal axis of the hindlimb bud is maintained

renal/urinary system
• dysgenesis of pelvic/urogenital organs
• bladder aplasia

reproductive system
• hypoplasia of external genitalia

skeleton
• defective fibula formation, with fibula aberrantly located medially or absent

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
physical disorder DOID:0080015 J:192045




Genotype
MGI:5643693
cn2
Allelic
Composition
Rspo3tm1Arte/Rspo3tm1Arte
Isl1tm1(cre)Sev/Isl1+
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Isl1tm1(cre)Sev mutation (1 available); any Isl1 mutation (33 available)
Rspo3tm1Arte mutation (0 available); any Rspo3 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

cardiovascular system
• myocardial wall thickness is diminished at E10
• poorly developed outflow tract
• poorly developed right ventricle
• in all mice

homeostasis/metabolism
• in all mice

muscle
• myocardial wall thickness is diminished at E10




Genotype
MGI:5643691
cn3
Allelic
Composition
Nkx2-5tm1Krc/Nkx2-5tm1Krc
Isl1tm1(cre)Sev/Isl1+
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Isl1tm1(cre)Sev mutation (1 available); any Isl1 mutation (33 available)
Nkx2-5tm1Krc mutation (0 available); any Nkx2-5 mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• early embryonic lethality at E10-E10.5

cardiovascular system
• foreshortened outflow tract
• treatment of pregnant females from E8 to E10 with LiCl results in septation of the outflow tract in embryos, although it fails to correct the alignment defects of the outflow tract
• loss of right ventricle
• treatment of pregnant females from E8 to E10 with LiCl results in a larger right ventricle




Genotype
MGI:7294563
cn4
Allelic
Composition
Isl1tm1(cre)Sev/Isl1+
Pax9tm1Rbal/Pax9tm1.1Hpt
Genetic
Background
involves: 129 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Isl1tm1(cre)Sev mutation (1 available); any Isl1 mutation (33 available)
Pax9tm1.1Hpt mutation (0 available); any Pax9 mutation (16 available)
Pax9tm1Rbal mutation (0 available); any Pax9 mutation (16 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• absent common carotid arteries in 9 of 9 mice
• in 1 of 9 mice

craniofacial
N
• unlike in germline null mice, cleft palate is not seen

endocrine/exocrine glands
• hypoplastic and absent from the normal position
• hypoplastic and absent from the normal position

hematopoietic system
• hypoplastic and absent from the normal position
• hypoplastic and absent from the normal position

immune system
• hypoplastic and absent from the normal position
• hypoplastic and absent from the normal position

limbs/digits/tail




Genotype
MGI:7294564
cn5
Allelic
Composition
Isl1tm1(cre)Sev/Isl1+
Msx1tm1Rilm/Msx1+
Pax9tm1Rbal/Pax9tm1.1Hpt
Genetic
Background
involves: 129 * CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Isl1tm1(cre)Sev mutation (1 available); any Isl1 mutation (33 available)
Msx1tm1Rilm mutation (1 available); any Msx1 mutation (18 available)
Pax9tm1.1Hpt mutation (0 available); any Pax9 mutation (16 available)
Pax9tm1Rbal mutation (0 available); any Pax9 mutation (16 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

skeleton
• ossification center is shorter
• angle between the greater and lesser horns is reduced

craniofacial
• unlike in germline null mice, cleft palate is not seen
• ossification center is shorter
• angle between the greater and lesser horns is reduced

limbs/digits/tail

cardiovascular system
• cervical origin in 2 of 8 neonates

respiratory system




Genotype
MGI:7562242
cn6
Allelic
Composition
Juntm4Wag/Juntm4Wag
Isl1tm1(cre)Sev/Isl1+
Genetic
Background
involves: 129P2/OlaHsd * 129S/Sv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Isl1tm1(cre)Sev mutation (1 available); any Isl1 mutation (33 available)
Juntm4Wag mutation (0 available); any Jun mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• mice are present at the expected Mendelian ratios at E14.5-P0, indicating normal embryonic survival

cardiovascular system
• at E14.5 to P0, seven of 22 (32%) embryos exhibit aortic arch artery remodeling defects, including interrupted aortic arch (IAA) type B, hypoplasia of the B segment of the aortic arch, and aberrant retro-esophageal right subclavian artery
• at E14.5 to P0, seven of 22 (32%) embryos exhibit aberrant retro-esophageal right subclavian artery
• at E14.5 to P0, seven of 22 (32%) embryos exhibit interrupted aortic arch (IAA) type B
• at E14.5 to P0, seven of 8 (88%) embryos exhibit outflow tract (OFT) defects, including ventricular septal defect (VSD), double outlet right ventricle, and semilunar valve hyperplasia
• a non-significant trend toward a decrease in proliferating pHH3+ cells and an increase in apoptotic TUNEL+ cells is noted in the OFT at E10.5
• at E14.5 to P0, seven of 8 (88%) embryos exhibit DORV
• at E14.5 to P0, seven of 8 (88%) embryos exhibit VSDs
• at E14.5 to P0, six of 8 (75%) embryos exhibit an aortic valve defect
• at E14.5 to P0, seven of 8 (88%) embryos exhibit a pulmonary valve defect
• at PO, pulmonary valve leaflets are enlarged and hyperplastic
• at E14.5 to P0, seven of 8 (88%) embryos exhibit semilunar valve hyperplasia
• however, atrioventricular (mitral and tricuspid) valves are unaffected

embryo
• at E14.5 to P0, seven of 22 (32%) embryos exhibit aortic arch artery remodeling defects, including interrupted aortic arch (IAA) type B, hypoplasia of the B segment of the aortic arch, and aberrant retro-esophageal right subclavian artery

craniofacial
• at E14.5 to P0, seven of 22 (32%) embryos exhibit aortic arch artery remodeling defects, including interrupted aortic arch (IAA) type B, hypoplasia of the B segment of the aortic arch, and aberrant retro-esophageal right subclavian artery




Genotype
MGI:7562004
cn7
Allelic
Composition
Juntm1Pa/Juntm4Wag
Isl1tm1(cre)Sev/Isl1+
Genetic
Background
involves: 129P2/OlaHsd * 129S/Sv * 129X1/SvJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Isl1tm1(cre)Sev mutation (1 available); any Isl1 mutation (33 available)
Juntm1Pa mutation (1 available); any Jun mutation (12 available)
Juntm4Wag mutation (0 available); any Jun mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• at E10.5, embryos show normal expression of Nfatc1 (an endocardial marker) relative to controls, suggesting normal endocardial formation
• a non-significant trend toward a decrease in proliferating pHH3+ cells and an increase in apoptotic TUNEL+ cells is noted in the cardiac outflow tract (OFT) at E10.5

embryo
N
• at E10.5, embryos show normal expression of Tfap2a during cardiac OFT development relative to controls, suggesting normal cardiac neural crest cell migration




Genotype
MGI:7343918
cn8
Allelic
Composition
Bcortm1.1Vjba/Y
Isl1tm1(cre)Sev/Isl1+
Genetic
Background
involves: 129S1/Sv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bcortm1.1Vjba mutation (1 available); any Bcor mutation (21 available)
Isl1tm1(cre)Sev mutation (1 available); any Isl1 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• aortic arch abnormalities in 13% of hearts
• at E13.5 in 65% of embryos

limbs/digits/tail
• show simple or complex syndactyly of the second and third digits in 4 of 17 embryos at E14.5

mortality/aging
• begin to see decrease in numbers after E13.5




Genotype
MGI:7343919
cn9
Allelic
Composition
Bcortm1.1Vjba/Bcor+
Isl1tm1(cre)Sev/Isl1+
Genetic
Background
involves: 129S1/Sv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bcortm1.1Vjba mutation (1 available); any Bcor mutation (21 available)
Isl1tm1(cre)Sev mutation (1 available); any Isl1 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• at E13.5 in 7% of embryos

mortality/aging
• only 44% of expected mice survive to weaning




Genotype
MGI:3625139
cn10
Allelic
Composition
Bmpr1atm2.1Bhr/Bmpr1atm2.2Bhr
Isl1tm1(cre)Sev/Isl1+
Genetic
Background
involves: 129S4/SvJae * 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bmpr1atm2.1Bhr mutation (1 available); any Bmpr1a mutation (89 available)
Bmpr1atm2.2Bhr mutation (0 available); any Bmpr1a mutation (89 available)
Isl1tm1(cre)Sev mutation (1 available); any Isl1 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
embryo
• by E11.5 ectopic outgrowths were observed on the ventral surface of the hindlimb bud
• at E10, hindlimb buds were smaller

mortality/aging
• mutants were recovered at mendelian frequencies at E10.5
• began to be lost by E11.5 and no live mutant were recovered at E14.5

cardiovascular system
• abnormalities of outflow tract and right ventricle was evident by E8.5
• at E13.5 severe abnormalities of outflow tract formation with evident of persistent truncus arteriosus and underdeveloped valves
• proliferation of ventricular myocardium in the free wall and septum was also decreased in mutants relative to controls
• decreased apoptosis in outflow tract cushions and increased apoptosis atop the ventricular septum

muscle
• proliferation of ventricular myocardium in the free wall and septum was also decreased in mutants relative to controls
• decreased apoptosis in outflow tract cushions and increased apoptosis atop the ventricular septum

limbs/digits/tail
• by E11.5 ectopic outgrowths were observed on the ventral surface of the hindlimb bud
• at E10, hindlimb buds were smaller
• by E13.5 hindlimb formation was severely abnormal

cellular
• proliferation of ventricular myocardium in the free wall and septum was also decreased in mutants relative to controls
• decreased apoptosis in outflow tract cushions and increased apoptosis atop the ventricular septum
• proliferation of developing hindlimb buds was severely decreased




Genotype
MGI:3831923
cn11
Allelic
Composition
Dvl3tm1Awb/Dvl3tm1Awb
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Isl1tm1(cre)Sev/Isl1+
Genetic
Background
involves: 129S4/SvJaeSor * 129S6/SvEvTac * Black Swiss
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dvl3tm1Awb mutation (1 available); any Dvl3 mutation (38 available)
Gt(ROSA)26Sortm1Sor mutation (8 available); any Gt(ROSA)26Sor mutation (944 available)
Isl1tm1(cre)Sev mutation (1 available); any Isl1 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• at E10.5, E14.5 and E18.5, secondary heart field development is normal




Genotype
MGI:5444492
cn12
Allelic
Composition
Isl1tm1(cre)Sev/Isl1+
Tg(CAG-lacZ,-BMPR1A*,-EGFP)1Mis/0
Genetic
Background
involves: 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Isl1tm1(cre)Sev mutation (1 available); any Isl1 mutation (33 available)
Tg(CAG-lacZ,-BMPR1A*,-EGFP)1Mis mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• membranous defect




Genotype
MGI:5444491
cn13
Allelic
Composition
Irx3tm3Hui/Irx3tm3Hui
Irx5tm3Hui/Irx5tm3Hui
Isl1tm1(cre)Sev/Isl1+
Genetic
Background
involves: 129S/Sv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Irx3tm3Hui mutation (0 available); any Irx3 mutation (24 available)
Irx5tm3Hui mutation (0 available); any Irx5 mutation (30 available)
Isl1tm1(cre)Sev mutation (1 available); any Isl1 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• phenocopies abnormalities seen in germ line double null mice
• absence of the dorsal mesenchymal protrusion and the septum primum
• appears to be due to a defect in the fusion between the atrioventricular endocardial cushions and the dorsal mesenchymal protrusion
• atrioventricular canal defect




Genotype
MGI:3639731
cn14
Allelic
Composition
Fgf8tm2Moon/Fgf8tm1Mrc
Isl1tm1(cre)Sev/Isl1+
Genetic
Background
involves: 129S/Sv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgf8tm1Mrc mutation (0 available); any Fgf8 mutation (18 available)
Fgf8tm2Moon mutation (0 available); any Fgf8 mutation (18 available)
Isl1tm1(cre)Sev mutation (1 available); any Isl1 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• severely affected mutants (35%) die by E10; most (65%) survive to birth

embryo
• at E8.75 -10.5, surviving mutants have small pharyngeal arches

cellular
• excess apoptotic cells are detected at the 7-9 somite stage in ventral endoderm and adjacent smooth muscle

cardiovascular system
• conotruncal cushions are hypocellular compared to controls; fusion of cushions to form AP septum is delayed in mutants
• 100% of E18.5/newborns have PTA
• at E8.75 -10.5, surviving mutants have severe right ventricle hypoplasia

craniofacial
• at E8.75 -10.5, surviving mutants have small pharyngeal arches




Genotype
MGI:3689403
cn15
Allelic
Composition
Smotm1Amc/Smotm2Amc
Isl1tm1(cre)Sev/Isl1+
Genetic
Background
involves: 129S/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Isl1tm1(cre)Sev mutation (1 available); any Isl1 mutation (33 available)
Smotm1Amc mutation (1 available); any Smo mutation (39 available)
Smotm2Amc mutation (1 available); any Smo mutation (39 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

cardiovascular system
• E10 embryos show an absence of the left 6th aortic arch although the right 6th arch is normal
• outflow tracts are shortened by about 17%, 18% and 22% at E10.5, E11.5, and E12.5, respectively
• exhibit increased apoptosis in outflow tract myocardium at E10
• seen in 19 of 20 mutants at E18.5
• seen in 1 of 20 mutants at E18.5
• E12.5 and E18.5 hearts show atrial septal defects
• ventricular septal defects

embryo
• E10 embryos show an absence of the left 6th aortic arch although the right 6th arch is normal
• marker analysis indicates that cardiac neural crest cells are present in the pharyngeal arches and the outflow tract but do not penetrate the outflow tract to the same extent as in wild-type

craniofacial
• E10 embryos show an absence of the left 6th aortic arch although the right 6th arch is normal

cellular
• marker analysis indicates that cardiac neural crest cells are present in the pharyngeal arches and the outflow tract but do not penetrate the outflow tract to the same extent as in wild-type




Genotype
MGI:3829040
cn16
Allelic
Composition
Fgf8tm1Mrc/Fgf8tm2Moon
Isl1tm1(cre)Sev/Isl1+
Genetic
Background
involves: 129S/Sv * Black Swiss * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgf8tm1Mrc mutation (0 available); any Fgf8 mutation (18 available)
Fgf8tm2Moon mutation (0 available); any Fgf8 mutation (18 available)
Isl1tm1(cre)Sev mutation (1 available); any Isl1 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• in explants no cells manage to successfully undergo endothelial to mesenchymal transformation
• outflow tracts are short and abnormally angulated
• outflow tract cushions contain less cardiac jelly and fewer mesenchymal cells
• proximal outflow tract cushions are thinner and contain fewer cells while distal cushions are thinner but do not display a change in cell density
• all show type III PTA (the outflow tract is unseptated along its entire proximodstal extent)




Genotype
MGI:6406420
cn17
Allelic
Composition
Epha4tm1.1Bzh/Epha4tm1.1Bzh
Isl1tm1(cre)Sev/Isl1+
Tg(Hlxb9-GFP)1Tmj/0
Genetic
Background
involves: 129S/Sv * Black Swiss * C57BL/6J * CD-1 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Epha4tm1.1Bzh mutation (1 available); any Epha4 mutation (66 available)
Isl1tm1(cre)Sev mutation (1 available); any Isl1 mutation (33 available)
Tg(Hlxb9-GFP)1Tmj mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• embryos show an increase in the number of abducens nerve bundles following exit from the hindbrain, reductions in both abducens nerve length and diameter at the orbit and larger wandering abducens nerve bundles that exhibit enhanced nerve pausing at the midpoint decision within the abducens fasciculation region
• however, trochlear nerve and first cervical spine projections are normal
• abducens nerve length is reduced and nerve diameter is thinner near the orbit in embryos




Genotype
MGI:7562245
cn18
Allelic
Composition
Isl1tm1(cre)Sev/Isl1+
Juntm4Wag/Jun+
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Isl1tm1(cre)Sev mutation (1 available); any Isl1 mutation (33 available)
Juntm4Wag mutation (0 available); any Jun mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• at E14.5 to P0, a single embryo (1 of 22) shows IAA type B
• however, no other OFT or aortic arch abnormalities are observed





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last database update
05/14/2024
MGI 6.23
The Jackson Laboratory