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Phenotypes Associated with This Genotype
Genotype
MGI:6460330
Allelic
Composition
Ldb1tm1Lmgd/Ldb1tm2Lmgd
H2az2Tg(Wnt1-cre)11Rth/H2az2+
Genetic
Background
involves: C57BL/6J * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
H2az2Tg(Wnt1-cre)11Rth mutation (2 available); any H2az2 mutation (25 available)
Ldb1tm1Lmgd mutation (0 available); any Ldb1 mutation (35 available)
Ldb1tm2Lmgd mutation (0 available); any Ldb1 mutation (35 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die shortly after birth

craniofacial
N
• face development is grossly unaffected; neural crest-derived cells show normal distribution in all facial primordia at E10.5
• appearance of diastema teeth on the upper jaw
• a loss of molars is observed in the upper jaw
• lower molars are developmentally arrested
• at E13.5, a small localized decrease in mesenchymal cell proliferation is seen in the medial area of the anterior palate
• however, palatal mesenchyme shows no significant differences in apoptosis relative to controls
• starting at E13.5, the palatal shelf has an abnormal shape being more blunt and wider at the bottom; this is more pronounced in the anterior and middle levels than in the posterior level
• however, no adhesion between the palatal shelf and the tongue or oral epithelium is observed
• starting at E14.5, the palatal shelves are smaller in the anterior and posterior palate
• all mice exhibit fully cleft secondary palate at birth
• at E14.5, the middle palate and the posterior palate remain vertical, whereas the anterior palate is normally elevated above the tongue
• at E18.5, the posterior palate fails to elevate above the tongue, whereas the middle palate appears to have initiated re-orientation as shown by the presence of a protrusion on the medial side of the palatal shelf
• expression of Wnt5a, Pax9 and Osr2, which regulate palatal shelf elevation, is altered
• defect in middle/posterior palatal shelf elevation is not due to mechanical hindrance by the tongue
• at E14.5 and E18.5, the tongue is abnormally tall
• however, in vitro head culture assays show that the defect in middle/posterior palatal shelf elevation is not due to interference by the tongue

growth/size/body
• appearance of diastema teeth on the upper jaw
• a loss of molars is observed in the upper jaw
• lower molars are developmentally arrested
• at E13.5, a small localized decrease in mesenchymal cell proliferation is seen in the medial area of the anterior palate
• however, palatal mesenchyme shows no significant differences in apoptosis relative to controls
• starting at E13.5, the palatal shelf has an abnormal shape being more blunt and wider at the bottom; this is more pronounced in the anterior and middle levels than in the posterior level
• however, no adhesion between the palatal shelf and the tongue or oral epithelium is observed
• starting at E14.5, the palatal shelves are smaller in the anterior and posterior palate
• all mice exhibit fully cleft secondary palate at birth
• at E14.5, the middle palate and the posterior palate remain vertical, whereas the anterior palate is normally elevated above the tongue
• at E18.5, the posterior palate fails to elevate above the tongue, whereas the middle palate appears to have initiated re-orientation as shown by the presence of a protrusion on the medial side of the palatal shelf
• expression of Wnt5a, Pax9 and Osr2, which regulate palatal shelf elevation, is altered
• defect in middle/posterior palatal shelf elevation is not due to mechanical hindrance by the tongue
• at E14.5 and E18.5, the tongue is abnormally tall
• however, in vitro head culture assays show that the defect in middle/posterior palatal shelf elevation is not due to interference by the tongue

digestive/alimentary system
• at E13.5, a small localized decrease in mesenchymal cell proliferation is seen in the medial area of the anterior palate
• however, palatal mesenchyme shows no significant differences in apoptosis relative to controls
• starting at E13.5, the palatal shelf has an abnormal shape being more blunt and wider at the bottom; this is more pronounced in the anterior and middle levels than in the posterior level
• however, no adhesion between the palatal shelf and the tongue or oral epithelium is observed
• starting at E14.5, the palatal shelves are smaller in the anterior and posterior palate
• all mice exhibit fully cleft secondary palate at birth
• at E14.5, the middle palate and the posterior palate remain vertical, whereas the anterior palate is normally elevated above the tongue
• at E18.5, the posterior palate fails to elevate above the tongue, whereas the middle palate appears to have initiated re-orientation as shown by the presence of a protrusion on the medial side of the palatal shelf
• expression of Wnt5a, Pax9 and Osr2, which regulate palatal shelf elevation, is altered
• defect in middle/posterior palatal shelf elevation is not due to mechanical hindrance by the tongue
• at E14.5 and E18.5, the tongue is abnormally tall
• however, in vitro head culture assays show that the defect in middle/posterior palatal shelf elevation is not due to interference by the tongue

skeleton
• appearance of diastema teeth on the upper jaw
• a loss of molars is observed in the upper jaw
• lower molars are developmentally arrested


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)
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last database update
01/06/2026
MGI 6.24
The Jackson Laboratory