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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Pax2-cre)1Akg
transgene insertion 1, Andrew K Groves
MGI:3046196
Summary 14 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Dicer1tm1Bdh/Dicer1tm1Bdh
Tg(Pax2-cre)1Akg/0
involves: 129 MGI:7439354
cn2
Bhlhe22tm2.1Meg/Bhlhe22tm2.1Meg
Tg(Pax2-cre)1Akg/0
involves: 129 MGI:4440933
cn3
Pdss2tm1.1Jdhu/Pdss2tm1.2Jdhu
Tg(Pax2-cre)1Akg/0
involves: 129 * C57BL/6N * FVB/N MGI:5304567
cn4
Tbx1tm2.1Bem/Tbx1tm2.2Bem
Tg(Pax2-cre)1Akg/0
involves: 129 * C57BL/6 * SJL MGI:3703706
cn5
Gt(ROSA)26Sortm1(Tbx1/GFP)Bem/Gt(ROSA)26Sor+
Tg(Pax2-cre)1Akg/0
involves: 129 * C57BL/6 * SJL MGI:5551751
cn6
Rbpjtm1Hon/Rbpjtm1Hon
Tg(Pax2-cre)1Akg/0
involves: 129P2/OlaHsd MGI:3713804
cn7
Notch1tm1Con/Notch1tm1Grid
Tg(Pax2-cre)1Akg/0
involves: 129S1/Sv * 129X1/SvJ MGI:3713803
cn8
Slc12a2tm1.1Jheb/Slc12a2tm1.1Jheb
Tbx1tm6(cre)Bld/Tbx1+
Tg(Pax2-cre)1Akg/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:5538349
cn9
Hgftm1Jmw/Hgftm1Jmw
Tg(Pax2-cre)1Akg/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CD-1 MGI:6446739
cn10
Chd7tm1.1Dmm/Chd7tm1.1Dmm
Tg(Pax2-cre)1Akg/0
involves: 129S1/SvImJ * 129S6/SvEvTac * C57BL/6 MGI:7518606
cn11
Gata3tm1.1Gan/Gata3tm1.1Gan
Tg(Pax2-cre)1Akg/0
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6Ncr MGI:5518952
cn12
Gata3tm1.1Gan/Gata3+
Tg(Pax2-cre)1Akg/0
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6Ncr MGI:5518953
cn13
Tg(Pax2-cre)1Akg/0
Vangl2tm1.2Mdea/Vangl2tm2.1Mdea
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:5552006
cn14
Chd7Gt(S20-7E1)Sor/Chd7tm1.1Dmm
Tg(Pax2-cre)1Akg/0
involves: 129S * C57BL/6 MGI:7518554


Genotype
MGI:7439354
cn1
Allelic
Composition
Dicer1tm1Bdh/Dicer1tm1Bdh
Tg(Pax2-cre)1Akg/0
Genetic
Background
involves: 129
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dicer1tm1Bdh mutation (4 available); any Dicer1 mutation (96 available)
Tg(Pax2-cre)1Akg mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice exhibit late embryonic lethality at E18.5

craniofacial
• at E17.5, mice exhibit severe craniofacial dysmorphism, including a secondary palatal cleft
• however, orofacial development is not affected prior to E11.5
• at E17.5, mice show complete loss or abrogated development of several cranial neural crest cell (CNC)-derived bones in the viscerocranium, anterior cranial vault, and prechordal skull base
• in contrast, mesoderm-derived skeletal elements of the posterior skull, including the parietal, intraparietal, petrous temporal, basioccipital, exoccipital and supraoccipital, are normal
• at E17.5, the presphenoid, alisphenoid, and orbitosphenoid were absent from the cranial base
• at E17.5, the basisphenoid of the cranial base shows impaired growth
• at E17.5, the medial portion of the frontal bones in the calvaria shows impaired growth
• slight frontal bossing at E17.5
• at E17.5, the alisphenoid is absent
• at E17.5, the orbitosphenoid is absent
• at E17.5, the presphenoid is absent
• at E17.5, the squamosal bone is absent
• reduction in cranial vault size at E17.5
• shallow orbits at E17.5
• at E17.5, the mandible is reduced in size
• at E17.5, the frontal process of the maxilla is reduced in size
• micrognathia at E17.5
• at E17.5, the palatine bones of the maxilla are absent
• at E17.5, the vomer is reduced in size
• at E17.5, the jugal (zygoma) bone is absent
• at E11.5, apoptotic (ApopTag+) cells are detected throughout the orofacial region, esp. in the developing palatal areas
• however, ApopTag+ cells are not observed in the palatal region at E17.5
• at E17.5, the presumptive secondary palate shows only limited mesenchymal condensation and a complete absence of mineralization in the truncated palatal shelves
• secondary palate development is arrested prior to mineralization around E13.5, with a significant increase in the expression levels of apoptotic markers Caspase 3 and Trp53 in palatal tissue esp. at E13.5
• expression levels for senescence marker Cdkn1a (p21) are increased at E11.5 and E13.5
• however, primary palate development and the initial stages of secondary palate formation appear unaffected
• at E16.5, palatal shelves exhibit arrested growth, remaining vertically oriented in position and are morphologically similar to the shelves of an E13.5 wild-type embryo
• at E16.5, intramembranous ossification is completely absent in the palatal shelf region
• in contrast, the nasal septal cartilage, which develops from the Pax2-Cre-negative frontonasal region, is present
• at E16.5, palatal shelves remain vertically oriented in position
• at ~E13.5, palatal shelves are vertically positioned along the side of the tongue but show a slight reduction in size
• midface hypoplasia at E17.5
• complete cleft of the secondary palate at E16.5 and E17.5

growth/size/body
• slight frontal bossing at E17.5
• at E17.5, the presumptive secondary palate shows only limited mesenchymal condensation and a complete absence of mineralization in the truncated palatal shelves
• secondary palate development is arrested prior to mineralization around E13.5, with a significant increase in the expression levels of apoptotic markers Caspase 3 and Trp53 in palatal tissue esp. at E13.5
• expression levels for senescence marker Cdkn1a (p21) are increased at E11.5 and E13.5
• however, primary palate development and the initial stages of secondary palate formation appear unaffected
• at E16.5, palatal shelves exhibit arrested growth, remaining vertically oriented in position and are morphologically similar to the shelves of an E13.5 wild-type embryo
• at E16.5, intramembranous ossification is completely absent in the palatal shelf region
• in contrast, the nasal septal cartilage, which develops from the Pax2-Cre-negative frontonasal region, is present
• at E16.5, palatal shelves remain vertically oriented in position
• at ~E13.5, palatal shelves are vertically positioned along the side of the tongue but show a slight reduction in size
• midface hypoplasia at E17.5
• complete cleft of the secondary palate at E16.5 and E17.5

digestive/alimentary system
• at E17.5, the presumptive secondary palate shows only limited mesenchymal condensation and a complete absence of mineralization in the truncated palatal shelves
• secondary palate development is arrested prior to mineralization around E13.5, with a significant increase in the expression levels of apoptotic markers Caspase 3 and Trp53 in palatal tissue esp. at E13.5
• expression levels for senescence marker Cdkn1a (p21) are increased at E11.5 and E13.5
• however, primary palate development and the initial stages of secondary palate formation appear unaffected
• at E16.5, palatal shelves exhibit arrested growth, remaining vertically oriented in position and are morphologically similar to the shelves of an E13.5 wild-type embryo
• at E16.5, intramembranous ossification is completely absent in the palatal shelf region
• in contrast, the nasal septal cartilage, which develops from the Pax2-Cre-negative frontonasal region, is present
• at E16.5, palatal shelves remain vertically oriented in position
• at ~E13.5, palatal shelves are vertically positioned along the side of the tongue but show a slight reduction in size
• complete cleft of the secondary palate at E16.5 and E17.5

skeleton
• at E17.5, mice show complete loss or abrogated development of several cranial neural crest cell (CNC)-derived bones in the viscerocranium, anterior cranial vault, and prechordal skull base
• in contrast, mesoderm-derived skeletal elements of the posterior skull, including the parietal, intraparietal, petrous temporal, basioccipital, exoccipital and supraoccipital, are normal
• at E17.5, the presphenoid, alisphenoid, and orbitosphenoid were absent from the cranial base
• at E17.5, the basisphenoid of the cranial base shows impaired growth
• at E17.5, the medial portion of the frontal bones in the calvaria shows impaired growth
• slight frontal bossing at E17.5
• at E17.5, the alisphenoid is absent
• at E17.5, the orbitosphenoid is absent
• at E17.5, the presphenoid is absent
• at E17.5, the squamosal bone is absent
• reduction in cranial vault size at E17.5
• shallow orbits at E17.5
• at E17.5, the mandible is reduced in size
• at E17.5, the frontal process of the maxilla is reduced in size
• micrognathia at E17.5
• at E17.5, the palatine bones of the maxilla are absent
• at E17.5, the vomer is reduced in size
• at E17.5, the jugal (zygoma) bone is absent
• at E16.5, intramembranous ossification is completely absent in the palatal shelf region
• in contrast, the nasal septal cartilage, which develops from the Pax2-Cre-negative frontonasal region, is present

vision/eye
• at E17.5, the orbitosphenoid is absent
• shallow orbits at E17.5
• exophthalmos due to shallow orbits at E17.5
• absence of eyelid formation at E17.5

nervous system
• slight cerebral hemorrhage at E17.5

hearing/vestibular/ear
• at E17.5, the tympanic ring is reduced in size

cellular
• at E11.5, the total number of EdU+ cells are markedly reduced in the region of the developing brain and first pharyngeal arch

cardiovascular system
• slight cerebral hemorrhage at E17.5




Genotype
MGI:4440933
cn2
Allelic
Composition
Bhlhe22tm2.1Meg/Bhlhe22tm2.1Meg
Tg(Pax2-cre)1Akg/0
Genetic
Background
involves: 129
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bhlhe22tm2.1Meg mutation (0 available); any Bhlhe22 mutation (12 available)
Tg(Pax2-cre)1Akg mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• resulting in skin lesions in most animals
• mice show excessive scratching in response to pruritic agents

integument
• animals display self-inflicted skin lesions




Genotype
MGI:5304567
cn3
Allelic
Composition
Pdss2tm1.1Jdhu/Pdss2tm1.2Jdhu
Tg(Pax2-cre)1Akg/0
Genetic
Background
involves: 129 * C57BL/6N * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pdss2tm1.1Jdhu mutation (0 available); any Pdss2 mutation (31 available)
Pdss2tm1.2Jdhu mutation (0 available); any Pdss2 mutation (31 available)
Tg(Pax2-cre)1Akg mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice die within 36 hours of life

nervous system
• at E14.5, mice exhibit ectopic apoptosis accompanying the progression of cerebellum hypoplasia
• at E12.5, radial glial cells in the cerebellum are fewer in number and have shorter processes compared to in wild-type mice
• fewer radial glial cells in the cerebellum at E12.5
• neurons are highly compacted close to the ventricular surface and leave the dorsal region devoid of cells unlike in wild-type mice
• small midbrain at E17.5
• hypoplasia is more severe at the vermis (midline region) than in cerebellar hemispheres
• cell stratification is disorganized
• cerebellum growth retardation begins at E12.5 and E14.5 due to decreased cell proliferation, increased ectopic apoptosis (beginning at E14.5), and impaired expansion of cerebellum volume
• at E14.5, expansion of the intermediate zone is delayed compared to in wild-type mice
• at E17.5
• at E17.5 and P0
• at E12.5, the subventricular zone has fewer and disorganized cells above the proliferating cell layers compared to in wild-type mice

craniofacial
• in all mice
• palatine shelves retain a vertical position and fail to fuse along the midline
• in 21 of 42

behavior/neurological
• in mice with normal palates

muscle
• at P0, lipid accumulates in the forelimb skeletal muscle

respiratory system

cellular
• at E18.5, cells of the cerebellum exhibit abnormal mitochondrial and autophagic-like vacuoles compared to in wild-type mice
• in cells of the cerebellum
• at E14.5, mice exhibit ectopic apoptosis accompanying the progression of cerebellum hypoplasia
• at E12.5, radial glial cells in the cerebellum are fewer in number and have shorter processes compared to in wild-type mice
• fewer radial glial cells in the cerebellum at E12.5
• neurons are highly compacted close to the ventricular surface and leave the dorsal region devoid of cells unlike in wild-type mice

skeleton
• in all mice
• palatine shelves retain a vertical position and fail to fuse along the midline

digestive/alimentary system
• palatine shelves retain a vertical position and fail to fuse along the midline
• in 21 of 42

growth/size/body
• palatine shelves retain a vertical position and fail to fuse along the midline
• in 21 of 42




Genotype
MGI:3703706
cn4
Allelic
Composition
Tbx1tm2.1Bem/Tbx1tm2.2Bem
Tg(Pax2-cre)1Akg/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tbx1tm2.1Bem mutation (0 available); any Tbx1 mutation (36 available)
Tbx1tm2.2Bem mutation (0 available); any Tbx1 mutation (36 available)
Tg(Pax2-cre)1Akg mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hearing/vestibular/ear
• at E10.5
• early otic vesicle development is normal; however, the structure is hypoplastic at E10.5
• in contrast, periotic mesenchyme development appears normal
• at E17.5, 12 of 16 mutant ears show complete failure of inner ear development while the remaining appear completely normal
• in contrast, formation of the otic capsule and development of middle ear ossicles and pinnae is clearly normal at E17.5 and in adulthood
• in 12 of 16 mutant inner ears
• in 12 of 16 mutant inner ears
• in 12 of 16 mutant inner ears
• at E17.5, 6 of 8 mutants show complete aplasia of inner ear sensory organs
• at E17.5, 6 of 8 mutant embryos display a severely hypoplastic inner ear
• severe hypoplasia is bilateral and present in 12/16 mutant ears
• at E17.5, the inner ear persists in a rudimentary otic vesicle stage
• 3 of 5 adults exhibit no hearing on either the left or right side, as determined by auditory brainstem response testing
• the remaining two adults display normal hearing, consistent with the incomplete penetrance of the inner ear phenotype noted at E17.5
• in 3 of 5 adult mutants

nervous system
• at E10.5, a smaller otic vesicle is surrounded by an expanded cochleovestibular ganglion
• at E11.5, the cochleovestibular ganglion is duplicated around the otic vesicle anterior-posterior midline

embryo
N
• at E10.5, mutants show normal invagination of the pharyngeal endoderm to form the future tubotympanic recess

craniofacial
N
• mutants survive in normal Mendelian ratios through adulthood and show normal craniofacial bone development at E17.5




Genotype
MGI:5551751
cn5
Allelic
Composition
Gt(ROSA)26Sortm1(Tbx1/GFP)Bem/Gt(ROSA)26Sor+
Tg(Pax2-cre)1Akg/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(Tbx1/GFP)Bem mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Pax2-cre)1Akg mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Thymic aplasia, nasal malformations, and eye, pharyngeal and ear defects in Gt(ROSA)26Sortm1(Tbx1/GFP)Bem/Gt(ROSA)26Sor+ Foxg1tm1(cre)Skm/Foxg1+ mice and microcephaly, ocular and ear defects in Gt(ROSA)26Sortm1(Tbx1/GFP)Bem/Gt(ROSA)26Sor+ Tg(Pax2-cre)1Akg/0 mice

mortality/aging

hearing/vestibular/ear
• hypoplastic to varying degrees, but enlarged in two instances
• fusion plates are not joined at E12.25
• however, they have partially recovered by E14.5
• enlarged at E14.5




Genotype
MGI:3713804
cn6
Allelic
Composition
Rbpjtm1Hon/Rbpjtm1Hon
Tg(Pax2-cre)1Akg/0
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rbpjtm1Hon mutation (2 available); any Rbpj mutation (193 available)
Tg(Pax2-cre)1Akg mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• embryos are normal at E12.5, but die at E13.5

renal/urinary system
• podocytes with WT1high expression do not develop in E12.5 cultures
• cultured E12.5 mtanephroi branch normally, but tubules positive for LTL (lectin) are not detected




Genotype
MGI:3713803
cn7
Allelic
Composition
Notch1tm1Con/Notch1tm1Grid
Tg(Pax2-cre)1Akg/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Notch1tm1Con mutation (3 available); any Notch1 mutation (117 available)
Notch1tm1Grid mutation (0 available); any Notch1 mutation (117 available)
Tg(Pax2-cre)1Akg mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• embryos are normal at E12.5, but die at E13.5

renal/urinary system
N
• metanephroi appear normal morphologically and histologically when cultured at E12.5

cardiovascular system




Genotype
MGI:5538349
cn8
Allelic
Composition
Slc12a2tm1.1Jheb/Slc12a2tm1.1Jheb
Tbx1tm6(cre)Bld/Tbx1+
Tg(Pax2-cre)1Akg/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Slc12a2tm1.1Jheb mutation (0 available); any Slc12a2 mutation (58 available)
Tbx1tm6(cre)Bld mutation (1 available); any Tbx1 mutation (36 available)
Tg(Pax2-cre)1Akg mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological

hearing/vestibular/ear
• collapse of the membranes of the vestibular compartments
• cristae degeneration




Genotype
MGI:6446739
cn9
Allelic
Composition
Hgftm1Jmw/Hgftm1Jmw
Tg(Pax2-cre)1Akg/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hgftm1Jmw mutation (1 available); any Hgf mutation (55 available)
Tg(Pax2-cre)1Akg mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hearing/vestibular/ear
• reduction in future strial intermediate cells

pigmentation
• reduction in future strial intermediate cells




Genotype
MGI:7518606
cn10
Allelic
Composition
Chd7tm1.1Dmm/Chd7tm1.1Dmm
Tg(Pax2-cre)1Akg/0
Genetic
Background
involves: 129S1/SvImJ * 129S6/SvEvTac * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Chd7tm1.1Dmm mutation (1 available); any Chd7 mutation (138 available)
Tg(Pax2-cre)1Akg mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hearing/vestibular/ear
• 57% shorter compared to controls
• region specific defects in innervation and patterning of the sensory epithelium
• in the middle region there is a narrowing of the epithelium with missing outer hair cells and a bifurcation of the direction of neuritic projections, with most neurites projecting towards the apex rather than the base
• severity of the phenotype in the middle region varies widely in severity
• some show undulating epithelium
• abundant supernumerary hair cells in the apex
• less frequent supernumerary hair cells in the middle section
• rarely see supernumerary hair cells in the base

nervous system
• abundant supernumerary hair cells in the apex
• less frequent supernumerary hair cells in the middle section
• rarely see supernumerary hair cells in the base
• disorganized spiral ganglion neurite projections in the apex of the cochlea




Genotype
MGI:5518952
cn11
Allelic
Composition
Gata3tm1.1Gan/Gata3tm1.1Gan
Tg(Pax2-cre)1Akg/0
Genetic
Background
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6Ncr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gata3tm1.1Gan mutation (0 available); any Gata3 mutation (32 available)
Tg(Pax2-cre)1Akg mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die shortly after birth

hearing/vestibular/ear
• short cochlea with no obvious turns with some degree of bifurcation at the apex region at E13.5
• prosensory domain development, as determined by marker expression, is disrupted
• however, initial cochleovestibular ganglion generation is normal
• disorganized, miniature, short cochlear duct with no obvious turns
• patchy formation of the organ of Corti-like structures, containing sometimes limited supporting cells either lacking or variable numbers of hair cells
• in some organ of Corti-like structures
• in some organ of Corti-like structures
• no obvious turns
• absent horizontal crista
• however, the anterior cristae seems normal

nervous system
• in some organ of Corti-like structures
• in some organ of Corti-like structures
• auditory fibers and projection defects
• however, neural fibers to the utricle and anterior cristae are normal
• loss of spiral ganglion nerves during early development
• however, initial cochleovestibular ganglion generation is normal
• missing inferior vestibular ganglion

cellular
• in the cochlear duct beyond the prosensory region at E12.5 and E13.5
• in the spiral ganglion nerves during early development




Genotype
MGI:5518953
cn12
Allelic
Composition
Gata3tm1.1Gan/Gata3+
Tg(Pax2-cre)1Akg/0
Genetic
Background
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6Ncr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gata3tm1.1Gan mutation (0 available); any Gata3 mutation (32 available)
Tg(Pax2-cre)1Akg mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body




Genotype
MGI:5552006
cn13
Allelic
Composition
Tg(Pax2-cre)1Akg/0
Vangl2tm1.2Mdea/Vangl2tm2.1Mdea
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Pax2-cre)1Akg mutation (2 available)
Vangl2tm1.2Mdea mutation (0 available); any Vangl2 mutation (34 available)
Vangl2tm2.1Mdea mutation (1 available); any Vangl2 mutation (34 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hearing/vestibular/ear
N
• cochlear length and number of turns are normal
• shifted out of the second and third outer hair cell rows and not centrally positioned between the hair cell lateral edges
• at P10 and P12, more pronounced in the apical turn
• more compact and incorrectly positioned compared with control mice
• reduced ABR amplitude
• however, the overall shape of the waveform is normal
• decreased amplitude of the distortion product

nervous system




Genotype
MGI:7518554
cn14
Allelic
Composition
Chd7Gt(S20-7E1)Sor/Chd7tm1.1Dmm
Tg(Pax2-cre)1Akg/0
Genetic
Background
involves: 129S * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Chd7Gt(S20-7E1)Sor mutation (1 available); any Chd7 mutation (138 available)
Chd7tm1.1Dmm mutation (1 available); any Chd7 mutation (138 available)
Tg(Pax2-cre)1Akg mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hearing/vestibular/ear
• severely malformed and hypoplastic





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last database update
11/12/2024
MGI 6.24
The Jackson Laboratory