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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Wnt7atm1Amc
targeted mutation 1, Andrew P McMahon
MGI:1857704
Summary 4 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Wnt7atm1Amc/Wnt7atm1Amc involves: 129S1/Sv MGI:2174809
cn2
Edil3Tg(Sox2-cre)1Amc/Edil3+
Wnt7atm1Amc/Wnt7atm1Amc
Wnt7btm1Parr/Wnt7btm2Amc
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA MGI:3831189
cn3
Tg(Nes-cre)1Kln/0
Wnt7atm1Amc/Wnt7atm1Amc
Wnt7btm1Parr/Wnt7btm2Amc
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3831188
cx4
En1tm1Alj/En1tm1Alj
Wnt7atm1Amc/Wnt7atm1Amc
Tg(Wnt1-En1)1Amc/0
either: (involves: 129S1/Sv * 129X1/SvJ) or (involves: 129S1/Sv * 129X1/SvJ * C57BL/6J) MGI:3718802


Genotype
MGI:2174809
hm1
Allelic
Composition
Wnt7atm1Amc/Wnt7atm1Amc
Genetic
Background
involves: 129S1/Sv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Wnt7atm1Amc mutation (1 available); any Wnt7a mutation (25 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
limbs/digits/tail
• interactions between signals for the two axes may be required for normal limb development
• abnormal limb development; dorsal to ventral transformation of cell fate in distal limbs including pigmented dermal thickenings resembling footpads, ventralized tendons, and ventralized sesamoid bones
• digit 5 is often missing or abnormal
• the ulna is often missing or abnormal

reproductive system
• anterior regions of the mutant reproductive tract display a fimbriated, ciliated epithelium typical of the proximal oviduct while posterior regions show a less elaborately folded mucosa composed of a simple columnar epithelium which resembles the isthmic region of the oviduct
• although regional differentiation occurs along the oviduct, normal elongation and coiling of the oviduct fail to occur
• no visibly coiled oviducts are present in newborn and adult female mutants
• mutant oviducts are shortened and uncoiled
• in female mutants, the mesenchymally derived uterine stroma is reduced such that the transverse and circular muscles, which are present but also reduced, lie in proximity to the endometrial epithelium
• adult female mutants show a nearly complete absence of uterine glands
• in female mutants, the neonatal uterus is significantly less muscular than that of wild-type females
• both epithelial and mesenchymal differentiation are disrupted in the mutant uterus
• epithelial differentiation is disrupted
• in female mutants, adult uteri are larger than at the neonatal stages but smaller than those of wild-type females
• in female mutants, the neonatal uterine wall is thinner and significantly less muscular than that of wild-type females
• the uterine radial diameter is less than half that of wild-type siblings
• in contrast, ovarian development is similar to that of wild-type females, as shown by normal follicular growth, ovulation and cycling in the adult
• mutant females are infertile due to abnormal development of the oviduct and uterus, both of which are Mullerian duct derivatives
• however, liveborn offspring are obtained from ovaries transplanted to recipient wild-type females
• adult mutant males are infertile due to the presence of non-regressed Mullerian ducts which prevent the exit of sperm

skeleton
• the ulna is often missing or abnormal

embryo
• although Mullerian ducts are present neonatally, the Mullerian duct derivatives of mutant newborn and adult females fail to differentiate properly (J:50342)
• the lumen of the Mullerian duct is expanded and the Mullerian duct mesenchyme is more condensed than in mice with conditional loss of Ctnnb1 in the Mullerian duct (J:171430)
• mutant males fail to undergo regression of the Mullerian duct due to absence of the receptor for Mullerian-inhibiting substance (J:50342)
• non-regressed Mullerian ducts appear as thin, undifferentiated tubes with no regional organization that run alongside the epididymis and the vas deferens from the testis to the urogenital sinus (J:50342)
• in addition, a second duct appears to prevent the vas deferens from making a proper connection at its distal end (J:50342)
• however, the testes and Wolffian duct derivatives (epididymis, vas deferens and seminal vesicle) appear normal and mature sperm fill the vas deferens (J:50342)

endocrine/exocrine glands
• adult female mutants show a nearly complete absence of uterine glands




Genotype
MGI:3831189
cn2
Allelic
Composition
Edil3Tg(Sox2-cre)1Amc/Edil3+
Wnt7atm1Amc/Wnt7atm1Amc
Wnt7btm1Parr/Wnt7btm2Amc
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Edil3Tg(Sox2-cre)1Amc mutation (5 available); any Edil3 mutation (42 available)
Wnt7atm1Amc mutation (1 available); any Wnt7a mutation (25 available)
Wnt7btm1Parr mutation (1 available); any Wnt7b mutation (17 available)
Wnt7btm2Amc mutation (1 available); any Wnt7b mutation (17 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all embryos die around E12.5 due to severe hemorrhaging within the central nervous system

cardiovascular system
• while vascularization has occurred within the ventral neural tube of control E10.5 embryos at the forelimb level, no such vascularization is observed in this region of mutant embryos
• in E12.5 embryos, endothelial cells and pericytes are absent from all ventral neural regions of the presumptive spinal cord except for in the floor plate
• in the dorsal neural tube of E12.5 embryos, endothelial cells and pericytes form abnormal clusters and enlarged lumens in the vascular structures present
• hemorrhaging is detected throughout the developing brain of E12.5 embryos
• hemorrhaging is detected throughout the developing spine of E12.5 embryos
• hemorrhaging and downregulation of the endothelial marker GLUT-1 suggest a defect in the blood brain barrier of developing embryos

nervous system
• hemorrhaging is detected throughout the developing brain of E12.5 embryos
• hemorrhaging is detected throughout the developing spine of E12.5 embryos
• hemorrhaging and downregulation of the endothelial marker GLUT-1 suggest a defect in the blood brain barrier of developing embryos




Genotype
MGI:3831188
cn3
Allelic
Composition
Tg(Nes-cre)1Kln/0
Wnt7atm1Amc/Wnt7atm1Amc
Wnt7btm1Parr/Wnt7btm2Amc
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Nes-cre)1Kln mutation (4 available)
Wnt7atm1Amc mutation (1 available); any Wnt7a mutation (25 available)
Wnt7btm1Parr mutation (1 available); any Wnt7b mutation (17 available)
Wnt7btm2Amc mutation (1 available); any Wnt7b mutation (17 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all embryos die around E12.5 due to severe hemorrhaging within the central nervous system

cardiovascular system
• the number of endothelial cells and pericytes present in the intraneural vascular plexus of E12.5 embryos is greatly reduced
• hemorrhaging is detected throughout the developing brain of E12.5 embryos
• hemorrhaging is detected throughout the developing spine of E12.5 embryos
• hemorrhaging and downregulation of the endothelial marker GLUT-1 suggest a defect in the blood brain barrier of developing embryos

nervous system
• hemorrhaging is detected throughout the developing brain of E12.5 embryos
• hemorrhaging is detected throughout the developing spine of E12.5 embryos
• hemorrhaging and downregulation of the endothelial marker GLUT-1 suggest a defect in the blood brain barrier of developing embryos




Genotype
MGI:3718802
cx4
Allelic
Composition
En1tm1Alj/En1tm1Alj
Wnt7atm1Amc/Wnt7atm1Amc
Tg(Wnt1-En1)1Amc/0
Genetic
Background
either: (involves: 129S1/Sv * 129X1/SvJ) or (involves: 129S1/Sv * 129X1/SvJ * C57BL/6J)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
En1tm1Alj mutation (2 available); any En1 mutation (32 available)
Tg(Wnt1-En1)1Amc mutation (0 available)
Wnt7atm1Amc mutation (1 available); any Wnt7a mutation (25 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• viability ranged from 3 weeks to beyond 4 months
• born in lower numbers than expected

limbs/digits/tail
• ventral surface of autopods is pigmented
• dorsal sesamoid processes in the 3rd digit
• no polydactyly
• some mice lack digit 5
• ectopic foot pads on digits 2, 3, and 4
• striations on the tips of digits 2, 3, and 5
• hardened foot pads
• dorsal surface of forelimbs with ventral surface characteristics





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