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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Zic3tm1Bca
targeted mutation 1, Brett Casey
MGI:2180720
Summary 8 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Zic3tm1Bca/Zic3tm1Bca involves: 129S7/SvEvBrd MGI:2180833
hm2
Zic3tm1Bca/Zic3tm1Bca involves: 129S7/SvEvBrd * C57BL/6 MGI:3618629
hm3
Zic3tm1Bca/Zic3tm1Bca involves: 129S7/SvEvBrd * C57BL/6J MGI:3618633
ht4
Zic3tm1Bca/Zic3+ involves: 129S7/SvEvBrd * C57BL/6 MGI:3618631
ot5
Zic3tm1Bca/Y involves: 129S7/SvEvBrd MGI:2180831
ot6
Zic3tm1Bca/Y involves: 129S7/SvEvBrd * C57BL/6 MGI:3618630
ot7
Zic3tm1Bca/Y involves: 129S7/SvEvBrd * C57BL/6J MGI:3618634
ot8
Zic3tm1Bca/Y involves: 129S7/SvEvBrd * Swiss MGI:3618632


Genotype
MGI:2180833
hm1
Allelic
Composition
Zic3tm1Bca/Zic3tm1Bca
Genetic
Background
involves: 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Zic3tm1Bca mutation (0 available); any Zic3 mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• despite normal numbers at E9.5, fewer than expected mice at E15.5 and weaning

cardiovascular system
• interruption with separate entrance of hepatic veins in some mice
• in 4 of 18 mice at E9.5
• sinisteral looping in some mice
• in some mice
• atrium isomerism in some mice
• in some mice

digestive/alimentary system
• in 5 of 58 mice at E15.5
• midline and right-sided stomach in some mice
• in some mice

embryo
• in 12 of 18 mice
• in 5 of 58 mice at E15.5
• in some mice at E9.5

growth/size/body
• in 12 of 18 mice
• in some mice at E9.5
• in 5 of 58 mice at E15.5
• laterality defects in 3 of 15 mice
• in some mice
• in some mice

craniofacial
• in 5 of 58 mice at E15.5

nervous system
• in 5 of 58 mice at E15.5
• in some mice at E9.5
• in 5 of 58 mice at E15.5

respiratory system
• pulmonary isomerism in some mice




Genotype
MGI:3618629
hm2
Allelic
Composition
Zic3tm1Bca/Zic3tm1Bca
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Zic3tm1Bca mutation (0 available); any Zic3 mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• about 30% of males are lost between birth and weaning
• significant lethality seen by E10.5 with continued loss of mice through birth
• this loss is somewhat less severe than in hemizygous males

embryo
• failure, delay, or abnormal direction of turning are seen
• some embryos that survive beyond the turning stage show rotation defects including abnormal thoracic and lumbar flexion, and/or abnormal looping of the distal tail (including the hindlimb buds)
• sidedness of the malformations appears to be random
• some embryos with no other gross abnormalities show evidence of growth delay
• seen in some embryos at E8.5
• at E9.5, failure of fusion is seen in some embryos in the midbrain-hindbrain region

nervous system
• seen in some embryos at E8.5
• at E9.5, failure of fusion is seen in some embryos in the midbrain-hindbrain region
• abnormal midbrain size and structure in some embryos
• abnormal forebrain size and structure in some embryos
• exencephalic mice have a disorganized basal ganglia
• exencephalic mice have an anteriorly displaced diencephalon
• exencephalic mice have a disorganized thalamus
• exencephalic mice have a disorganized hippocampus
• exencephalic mice have a disorganized cerebral cortex
• seen in exencephalic mice
• seen in a few stillborn pups
• seen in some pups delivered by Ceasarian sections
• xencephalic mice have rudimentary olfactory nerves

cardiovascular system
• a variety of cardiac defects are seen in a subset of embryos and these embryos always also have other abnormalities
• right aortic arch and interrupted aortic arch are seen in some embryos
• right aortic arch and interrupted aortic arch are seen in some embryos
• abnormal systemic venous connections
• one of the most common heart defects is dextro-transposition of the great arteries
• at E10.5 in several embryos the heart is positioned to the left side of the thorax, however in some abnormally turned embryos the heart is properly positioned at the midline and in 2 cases the heart is positioned to the right side of the thorax

respiratory system
• in a few embryos complete lung reversal is seen

digestive/alimentary system
• in some mice right sided stomach is seen

liver/biliary system
• in some mice reversed liver lobation is seen

immune system
• the spleen is always present but often hypoplastic

skeleton
• 10 null mice (includes males and females) had mostly unilateral axial skeletal defects
• partial rib duplications and inappropriately posterior sites of rib insertion are found
• partial duplications and partial fusions are seen
• apparent homeotic transformations

growth/size/body
• in some mice right sided stomach is seen
• some embryos with no other gross abnormalities show evidence of growth delay
• in a few embryos complete lung reversal is seen

hematopoietic system
• the spleen is always present but often hypoplastic




Genotype
MGI:3618633
hm3
Allelic
Composition
Zic3tm1Bca/Zic3tm1Bca
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Zic3tm1Bca mutation (0 available); any Zic3 mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• by E8.5 to E9.5 many of the most severely affected embryos (Type I) are beginning to be resorbed

embryo
• four types of mutant embryos are seen; Type I are the most severely affected (21.5% of hemizygous and homozygous mice), Type II are less severely affected (40.5%), Type III do not show defects until E8.0-E9.5 (16.5%), and Type IV do not show any gross defects at E6.5 through E9.5
• in Type I embryos abnormal expression of markers of the primitive streak suggest either failure to gastrulate or initiation of gastrulation that fails to progress normally
• in Type II embryos excess mesoderm formation is seen at the primitive streak, mesoderm is seen outside the primitive streak, and mesoderm is also found in the anterior of the embryo disrupting the connection of the anterior visceral endoderm with the underlying ectoderm
• in some Type II embryos no evidence of node-like tissue is seen at the midline, cellular accumulation is different on the left and right sides of the embryo, and the primitive streak is not in the midline
• by E8.0-E9.5, Type III embryos show signs of caudal truncation and/or abnormal somitogenesis
• Type III embryos all have a shortened posterior axis with variable degrees of caudal truncation from anterior head structures only to presence of the head and heart
• some mildly affected Type II embryos show signs of axial duplication
• some more severely affected Type II embryos stop developing around E8.5
• at E7.5-E7.5 the Type I embryos show significant developmental delay and remain at the epiblast or early streak stage
• in Type I embryos the epiblasts show signs of clefts and/or indistinct extraembryonic and embryonic ectoderm layers
• some mildly affected Type II embryos show asymmetric development of the posterior neural plate and the underlying mesoderm
• Type III embryos fail to develop a normal posterior neural plate
• poor differentiation of the neuroectoderm is seen in areas with increased cell number in the primitive streak
• variable degrees of axis duplication from partial formation of a second notochord through conjoined twinning occur
• isolated anterior and isolated posterior duplications are also seen and in some cases notochord tissue is absent from the trunk region
• in Type I embryos expression of markers for the primitive streak suggest that the anterior primitive streak and node are absent
• some less severely affected Type II embryos display an abnormal primitive streak with excess mesoderm formation, failure to properly elongate the primitive streak, and failure of the normal regionalization process
• Type III embryos do not display abnormalities until E8.0-E9.5 when an abnormal, rudimentary primitive streak region is seen
• at E9.0 in mildly affected embryos the primitive steak is thicker than in wild-type embryos, this increase in cell number may be unilateral or bilateral
• in Type I embryos expression of markers for the primitive streak suggest that the anterior primitive streak and node are absent
• in Type I embryos expression of markers for the primitive streak suggest that the anterior primitive streak and node are absent
• by E8.0-E9.5, Type III embryos show signs of caudal truncation and/or abnormal somitogenesis
• Type III embryos that do develop somites have reduced somite numbers and size
• asymmetries, most obviously seen in the somites, occur in about 10% of embryos probably as a result of partial axis duplications
• some less severely affected Type II embryos display a failure to properly elongate the primitive streak
• in embryos that have an intermediate phenotype (Type II) at mid streak and late streak a cells protrude into the amniotic cavity
• in Type III embryos the allantois is frequently small but the extraembryonic tissues are otherwise normal
• all markers of the anterior visceral endoderm are abnormal

nervous system
• some mildly affected Type II embryos show asymmetric development of the posterior neural plate and the underlying mesoderm
• Type III embryos fail to develop a normal posterior neural plate
• poor differentiation of the neuroectoderm is seen in areas with increased cell number in the primitive streak

cardiovascular system
• embryos with asymmetries often have abnormal cardiac looping

growth/size/body
• at E7.5-E7.5 the Type I embryos show significant developmental delay and remain at the epiblast or early streak stage




Genotype
MGI:3618631
ht4
Allelic
Composition
Zic3tm1Bca/Zic3+
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Zic3tm1Bca mutation (0 available); any Zic3 mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• about 30% of males are lost between birth and weaning

embryo
• failure, delay, or abnormal direction of turning are seen
• some embryos that survive beyond the turning stage show rotation defects including abnormal thoracic and lumbar flexion, and/or abnormal looping of the distal tail (including the hindlimb buds)
• sidedness of the malformations appears to be random
• some embryos with no other gross abnormalities show evidence of growth delay
• seen in some embryos at E8.5
• at E9.5, failure of fusion is seen in some embryos in the midbrain-hindbrain region

nervous system
• seen in some embryos at E8.5
• at E9.5, failure of fusion is seen in some embryos in the midbrain-hindbrain region
• abnormal midbrain size and structure in some embryos
• abnormal forebrain size and structure in some embryos
• exencephalic mice have a disorganized basal ganglia
• exencephalic mice have an anteriorly displaced diencephalon
• exencephalic mice have a disorganized thalamus
• exencephalic mice have a disorganized hippocampus
• exencephalic mice have a disorganized cerebral cortex
• seen in exencephalic mice
• seen in a few stillborn pups
• seen in some pups delivered by Ceasarian sections
• xencephalic mice have rudimentary olfactory nerves

cardiovascular system
• a variety of cardiac defects are seen in a subset of embryos and these embryos always also have other abnormalities
• an interrupted aortic arch is seen in some embryos
• a right aortic arch is seen in some embryos
• abnormal systemic venous connections
• one of the most common heart defects is dextro-transposition of the great arteries
• at E10.5 in several embryos the heart is positioned to the left side of the thorax, however in some abnormally turned embryos the heart is properly positioned at the midline and in 2 cases the heart is positioned to the right side of the thorax

respiratory system
• in a few embryos complete lung reversal is seen

digestive/alimentary system
• in some mice right sided stomach is seen

liver/biliary system
• in some mice reversed liver lobation is seen

immune system
• the spleen is always present but often hypoplastic

skeleton
• 2 heterozygous mice had mostly unilateral axial skeletal defects
• partial rib duplications and inappropriately posterior sites of rib insertion are found
• partial duplications and partial fusions are seen
• apparent homeotic transformations

limbs/digits/tail
• about 40% of heterozygous females have kinked tails

growth/size/body
• in some mice right sided stomach is seen
• some embryos with no other gross abnormalities show evidence of growth delay
• in a few embryos complete lung reversal is seen

hematopoietic system
• the spleen is always present but often hypoplastic




Genotype
MGI:2180831
ot5
Allelic
Composition
Zic3tm1Bca/Y
Genetic
Background
involves: 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Zic3tm1Bca mutation (0 available); any Zic3 mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• Background Sensitivity: no live born hemizygotes, unlike in crosses to C57BL/6 or outbred Swiss mice
• despite normal numbers at E9.5, fewer than expected mice at E15.5 and weaning

cardiovascular system
• in some mice
• interruption in some mice
• in 4 of 18 mice at E9.5
• sinisteral looping in some mice
• in some mice
• in some mice

craniofacial
• in 5 of 58 mice at E15.5

digestive/alimentary system
• in 5 of 58 mice at E15.5
• midline and right-sided stomach in some mice
• in some mice

embryo
• cells appear larger
• in 12 of 18 mice
• in 5 of 58 mice at E15.5
• the teardrop structure at the distal tip of the embryo is irregular and forms non-cohesive groups of node cells

growth/size/body
• in 12 of 18 mice
• in some mice at E9.5
• in 5 of 58 mice at E15.5
• laterality defects in 3 of 15 mice
• in some mice
• in some mice
• in some mice

nervous system
• in 5 of 58 mice at E15.5
• in 5 of 58 mice at E15.5

respiratory system
• in some mice

cellular




Genotype
MGI:3618630
ot6
Allelic
Composition
Zic3tm1Bca/Y
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Zic3tm1Bca mutation (0 available); any Zic3 mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• about 30% of males are lost between birth and weaning
• significant lethality seen by E10.5 with continued loss of mice through birth
• this loss is somewhat more severe than in homozygous females
• Background Sensitivity: lethality is more severe in crosses to C57BL/6 compared to outbred Swiss (viability of 0.26 versus 0.46, respectively)

embryo
• failure, delay, or abnormal direction of turning are seen
• some embryos that survive beyond the turning stage show rotation defects including abnormal thoracic and lumbar flexion, and/or abnormal looping of the distal tail (including the hindlimb buds)
• sidedness of the malformations appears to be random
• some embryos with no other gross abnormalities show evidence of growth delay
• seen in some embryos at E8.5
• at E9.5, failure of fusion is seen in some embryos in the midbrain-hindbrain region

nervous system
• seen in some embryos at E8.5
• at E9.5, failure of fusion is seen in some embryos in the midbrain-hindbrain region
• abnormal midbrain size and structure in some embryos
• abnormal forebrain size and structure in some embryos
• exencephalic mice have a disorganized basal ganglia
• exencephalic mice have an anteriorly displaced diencephalon
• exencephalic mice have a disorganized thalamus
• exencephalic mice have a disorganized hippocampus
• exencephalic mice have a disorganized cerebral cortex
• seen in exencephalic mice
• seen in a few stillborn pups
• seen in some pups delivered by Ceasarian sections
• xencephalic mice have rudimentary olfactory nerves

cardiovascular system
• a variety of cardiac defects are seen in a subset of embryos and these embryos always also have other abnormalities
• seen in some embryos
• seen in some embryos
• abnormal systemic venous connections
• one of the most common heart defects is dextro-transposition of the great arteries
• at E10.5 in several embryos the heart is positioned to the left side of the thorax, however in some abnormally turned embryos the heart is properly positioned at the midline and in 2 cases the heart is positioned to the right side of the thorax

respiratory system
• in a few embryos complete lung reversal is seen

digestive/alimentary system
• in some mice right sided stomach is seen

liver/biliary system
• in some mice reversed liver lobation is seen

immune system
• the spleen is always present but often hypoplastic

skeleton
• 10 null mice (includes males and females) had mostly unilateral axial skeletal defects
• partial rib duplications and inappropriately posterior sites of rib insertion are found
• partial duplications and partial fusions are seen
• apparent homeotic transformations

limbs/digits/tail
• all viable males have kinked tails

growth/size/body
• in some mice right sided stomach is seen
• some embryos with no other gross abnormalities show evidence of growth delay
• in a few embryos complete lung reversal is seen

hematopoietic system
• the spleen is always present but often hypoplastic




Genotype
MGI:3618634
ot7
Allelic
Composition
Zic3tm1Bca/Y
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Zic3tm1Bca mutation (0 available); any Zic3 mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• by E8.5 to E9.5 many of the most severely affected embryos (Type I) are beginning to be resorbed

embryo
• four types of mutant embryos are seen; Type I are the most severely affected (21.5% of hemizygous and homozygous mice), Type II are less severely affected (40.5%), Type III do not show defects until E8.0-E9.5 (16.5%), and Type IV do not show any gross defects at E6.5 through E9.5
• in Type I embryos abnormal expression of markers of the primitive streak suggest either failure to gastrulate or initiation of gastrulation that fails to progress normally
• in Type II embryos excess mesoderm formation is seen at the primitive streak, mesoderm is seen outside the primitive streak, and mesoderm is also found in the anterior of the embryo disrupting the connection of the anterior visceral endoderm with the underlying ectoderm
• in some Type II embryos no evidence of node-like tissue is seen at the midline, cellular accumulation is different on the left and right sides of the embryo, and the primitive streak is not in the midline
• by E8.0-E9.5, Type III embryos show signs of caudal truncation and/or abnormal somitogenesis
• Type III embryos all have a shortened posterior axis with variable degrees of caudal truncation from anterior head structures only to presence of the head and heart
• some mildly affected Type II embryos show signs of axial duplication
• some more severely affected Type II embryos stop developing around E8.5
• at E7.5-E7.5 the Type I embryos show significant developmental delay and remain at the epiblast or early streak stage
• in Type I embryos the epiblasts show signs of clefts and/or indistinct extraembryonic and embryonic ectoderm layers
• some mildly affected Type II embryos show asymmetric development of the posterior neural plate and the underlying mesoderm
• Type III embryos fail to develop a normal posterior neural plate
• poor differentiation of the neuroectoderm is seen in areas with increased cell number in the primitive streak
• variable degrees of axis duplication from partial formation of a second notochord through conjoined twinning occur
• isolated anterior and isolated posterior duplications are also seen and in some cases notochord tissue is absent from the trunk region
• in Type I embryos expression of markers for the primitive streak suggest that the anterior primitive streak and node are absent
• some less severely affected Type II embryos display an abnormal primitive streak with excess mesoderm formation, failure to properly elongate the primitive streak, and failure of the normal regionalization process
• Type III embryos do not display abnormalities until E8.0-E9.5 when an abnormal, rudimentary primitive streak region is seen
• at E9.0 in mildly affected embryos the primitive steak is thicker than in wild-type embryos, this increase in cell number may be unilateral or bilateral
• in Type I embryos expression of markers for the primitive streak suggest that the anterior primitive streak and node are absent
• in Type I embryos expression of markers for the primitive streak suggest that the anterior primitive streak and node are absent
• by E8.0-E9.5, Type III embryos show signs of caudal truncation and/or abnormal somitogenesis
• Type III embryos that do develop somites have reduced somite numbers and size
• asymmetries, most obviously seen in the somites, occur in about 10% of embryos probably as a result of partial axis duplications
• some less severely affected Type II embryos display a failure to properly elongate the primitive streak
• in embryos that have an intermediate phenotype (Type II) at mid streak and late streak a cells protrude into the amniotic cavity
• in Type III embryos the allantois is frequently small but the extraembryonic tissues are otherwise normal
• all markers of the anterior visceral endoderm are abnormal

nervous system
• some mildly affected Type II embryos show asymmetric development of the posterior neural plate and the underlying mesoderm
• Type III embryos fail to develop a normal posterior neural plate
• poor differentiation of the neuroectoderm is seen in areas with increased cell number in the primitive streak

cardiovascular system
• embryos with asymmetries often have abnormal cardiac looping

growth/size/body
• at E7.5-E7.5 the Type I embryos show significant developmental delay and remain at the epiblast or early streak stage




Genotype
MGI:3618632
ot8
Allelic
Composition
Zic3tm1Bca/Y
Genetic
Background
involves: 129S7/SvEvBrd * Swiss
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Zic3tm1Bca mutation (0 available); any Zic3 mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• significant lethality seen by E10.5 with continued loss of mice through birth
• Background Sensitivity: lethality is more severe in crosses to C57BL/6 compared to outbred Swiss (viability of 0.26 versus 0.46, respectively)





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last database update
04/23/2024
MGI 6.23
The Jackson Laboratory