About   Help   FAQ
Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Med23tm1c(KOMP)Wtsi
targeted mutation 1c, Wellcome Trust Sanger Institute
MGI:6502590
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Med23tm1c(KOMP)Wtsi/Med23tm1c(KOMP)Wtsi
H2az2Tg(Wnt1-cre)11Rth/H2az2+
involves: C57BL/6J * C57BL/6N * CBA/J MGI:7344053


Genotype
MGI:7344053
cn1
Allelic
Composition
Med23tm1c(KOMP)Wtsi/Med23tm1c(KOMP)Wtsi
H2az2Tg(Wnt1-cre)11Rth/H2az2+
Genetic
Background
involves: C57BL/6J * C57BL/6N * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
H2az2Tg(Wnt1-cre)11Rth mutation (2 available); any H2az2 mutation (26 available)
Med23tm1c(KOMP)Wtsi mutation (0 available); any Med23 mutation (75 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

behavior/neurological
• at P0, mice exhibit difficulty in feeding

respiratory system
• at P0, nasal cartilage is hypoplastic or absent
• at P0, mice exhibit difficulty in breathing

craniofacial
• by E14.5, severe craniofacial defects, including micrognathia and glossoptosis, are observed
• however, embryos appear morphologically normal until E12.5
• at P0, mice exhibit defects in bone development in the skull
• at E12.5, Meckels cartilage development is delayed
• at E14.5, Meckels cartilage appears to be loosely organized/packed
• at E12.5 and E14.5, Sox9 is upregulated in Meckels cartilage as well as in the mesenchyme surrounding Meckels cartilage
• by E14.5, Meckels cartilage is severely hypoplastic
• at P0, mice exhibit defects in cartilage development in the skull
• at P0, the frontal bone is underdeveloped
• at P0, the temporal bone is underdeveloped; otic bones are hypoplastic
• lower incisors are markedly smaller at E17.5
• at E17.5, upper incisors are developmentally delayed, having only reached the bell stage, whereas control upper incisors are transitioning from the late bell to eruption stage
• at P0, incisors are underdeveloped
• upper and lower molars are developmentally delayed at the bud stage at E14.5 and early bell stage at E17.5
• at P0, the mandible and condylar cartilage are hypoplastic
• at P0, the mandibular symphysis is absent
• at E14.5 and P0, lower jaw is smaller than normal
• at P0, the mandible is still hypoplastic
• micrognathia is detected at E14.5 and becomes more severe at P0
• at E14.5, palatine bones are absent
• Sox9 RNA and protein are upregulated in the frontonasal prominence
• mesenchymal cell proliferation is significantly reduced in E12.5 palatal shelves, resulting in lower cell density and smaller palatal shelves with limited ability to grow and fuse by E14.5
• at E12.5 and E14.5, Sox9 protein (an early marker of migratory NCCs and a master regulator of chondrogenesis) is ectopically expressed in the palatal shelves
• at E12.5, beta-catenin is downregulated in the palatal mesenchyme along with upregulated Sox9 expression and enhanced Sox9 binding to beta-catenin; Lef1 and Ccnd1 (downstream targets of beta-catenin) are also downregulated in the palatal shelves
• mesenchymal cell proliferation is significantly reduced in E12.5 palatal shelves, resulting in lower cell density and smaller palatal shelves with limited ability to grow and fuse by E14.5
• however, no changes in apoptosis are detected at E12.5 or E14.5
• at E14.5 and E17.5, the anterior palatal shelves are hypoplastic and unfused
• 72 hr after ex vivo roller culture, the palatal shelves develop rugae but remain separated and unfused, indicating that cleft palate is independent of tongue development or position
• at E14.5 and E17.5, the anterior palatal shelves are hypoplastic
• at E14.5, the volume of palatal shelves is significantly reduced
• Sox9 RNA and protein are upregulated in the NCCs colonizing the first pharyngeal arch between E9.5 and E11.5
• at E14.5, palatal shelves remain separated by the tongue
• by E17.5, the anterior palatal shelves have elevated above the tongue but still remain far apart
• in posterior sections, the palatal shelves grow vertically beside the tongue, fail to elevate and remain separated by the tongue
• at E17.5, the tongue is misshapen
• glossoptosis is detected at E14.5 and becomes more severe at P0
• at P0, nasal cartilage is hypoplastic or absent

skeleton
• at P0, mice exhibit defects in bone development in the skull
• at E12.5, Meckels cartilage development is delayed
• at E14.5, Meckels cartilage appears to be loosely organized/packed
• at E12.5 and E14.5, Sox9 is upregulated in Meckels cartilage as well as in the mesenchyme surrounding Meckels cartilage
• by E14.5, Meckels cartilage is severely hypoplastic
• at P0, mice exhibit defects in cartilage development in the skull
• at P0, the frontal bone is underdeveloped
• at P0, the temporal bone is underdeveloped; otic bones are hypoplastic
• lower incisors are markedly smaller at E17.5
• at E17.5, upper incisors are developmentally delayed, having only reached the bell stage, whereas control upper incisors are transitioning from the late bell to eruption stage
• at P0, incisors are underdeveloped
• upper and lower molars are developmentally delayed at the bud stage at E14.5 and early bell stage at E17.5
• at P0, the mandible and condylar cartilage are hypoplastic
• at P0, the mandibular symphysis is absent
• at E14.5 and P0, lower jaw is smaller than normal
• at P0, the mandible is still hypoplastic
• micrognathia is detected at E14.5 and becomes more severe at P0
• at E14.5, palatine bones are absent
• at P0, nasal cartilage is hypoplastic or absent

hearing/vestibular/ear

digestive/alimentary system
• mesenchymal cell proliferation is significantly reduced in E12.5 palatal shelves, resulting in lower cell density and smaller palatal shelves with limited ability to grow and fuse by E14.5
• at E12.5 and E14.5, Sox9 protein (an early marker of migratory NCCs and a master regulator of chondrogenesis) is ectopically expressed in the palatal shelves
• at E12.5, beta-catenin is downregulated in the palatal mesenchyme along with upregulated Sox9 expression and enhanced Sox9 binding to beta-catenin; Lef1 and Ccnd1 (downstream targets of beta-catenin) are also downregulated in the palatal shelves
• mesenchymal cell proliferation is significantly reduced in E12.5 palatal shelves, resulting in lower cell density and smaller palatal shelves with limited ability to grow and fuse by E14.5
• however, no changes in apoptosis are detected at E12.5 or E14.5
• at E14.5 and E17.5, the anterior palatal shelves are hypoplastic and unfused
• 72 hr after ex vivo roller culture, the palatal shelves develop rugae but remain separated and unfused, indicating that cleft palate is independent of tongue development or position
• at E14.5 and E17.5, the anterior palatal shelves are hypoplastic
• at E14.5, the volume of palatal shelves is significantly reduced
• at E14.5, palatal shelves remain separated by the tongue
• by E17.5, the anterior palatal shelves have elevated above the tongue but still remain far apart
• in posterior sections, the palatal shelves grow vertically beside the tongue, fail to elevate and remain separated by the tongue
• at E17.5, the tongue is misshapen
• glossoptosis is detected at E14.5 and becomes more severe at P0

growth/size/body
• lower incisors are markedly smaller at E17.5
• at E17.5, upper incisors are developmentally delayed, having only reached the bell stage, whereas control upper incisors are transitioning from the late bell to eruption stage
• at P0, incisors are underdeveloped
• upper and lower molars are developmentally delayed at the bud stage at E14.5 and early bell stage at E17.5
• mesenchymal cell proliferation is significantly reduced in E12.5 palatal shelves, resulting in lower cell density and smaller palatal shelves with limited ability to grow and fuse by E14.5
• at E12.5 and E14.5, Sox9 protein (an early marker of migratory NCCs and a master regulator of chondrogenesis) is ectopically expressed in the palatal shelves
• at E12.5, beta-catenin is downregulated in the palatal mesenchyme along with upregulated Sox9 expression and enhanced Sox9 binding to beta-catenin; Lef1 and Ccnd1 (downstream targets of beta-catenin) are also downregulated in the palatal shelves
• mesenchymal cell proliferation is significantly reduced in E12.5 palatal shelves, resulting in lower cell density and smaller palatal shelves with limited ability to grow and fuse by E14.5
• however, no changes in apoptosis are detected at E12.5 or E14.5
• at E14.5 and E17.5, the anterior palatal shelves are hypoplastic and unfused
• 72 hr after ex vivo roller culture, the palatal shelves develop rugae but remain separated and unfused, indicating that cleft palate is independent of tongue development or position
• at E14.5 and E17.5, the anterior palatal shelves are hypoplastic
• at E14.5, the volume of palatal shelves is significantly reduced
• at E14.5, palatal shelves remain separated by the tongue
• by E17.5, the anterior palatal shelves have elevated above the tongue but still remain far apart
• in posterior sections, the palatal shelves grow vertically beside the tongue, fail to elevate and remain separated by the tongue
• at E17.5, the tongue is misshapen
• glossoptosis is detected at E14.5 and becomes more severe at P0
• at P0, nasal cartilage is hypoplastic or absent

embryo
N
• neural crest cell migration is normal at E10.5
• Sox9 RNA and protein are upregulated in the NCCs colonizing the first pharyngeal arch between E9.5 and E11.5

nervous system
N
• neural crest cell (NCC) differentiation into neurons of the peripheral nervous system is normal at E10.5

cellular
N
• neural crest cell (NCC) migration and early neuronal differentiation is normal at E10.5





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)
Citing These Resources
Funding Information
Warranty Disclaimer, Privacy Notice, Licensing, & Copyright
Send questions and comments to User Support.
last database update
12/10/2024
MGI 6.24
The Jackson Laboratory