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Phenotypes Associated with This Genotype
Genotype
MGI:3038250
Allelic
Composition
Ddr1tm1Wfv/Ddr1tm1Wfv
Genetic
Background
either: (involves: (129S1/Sv * 129X1/SvJ) or (involves: 129S1/Sv * 129X1/SvJ * ICR) or (involves: 129S1/Sv * 129X1/SvJ * C57BL/6)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ddr1tm1Wfv mutation (0 available); any Ddr1 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• the mammary epithelium of virgin mice was hyperproliferative
• the mutant mammary glands displayed enlarged terminal end buds due to aberrant ductal growth
• the number of secondary ducts was increased, the ducts had wider lumens, and significantly larger amounts of extracellular matrix were deposited around the ducts
• during pregnancy, loss of encoded protein perturbed the lobuloalveolar proliferation and differentiation, resulting in a large number of alveoli that were unable to secrete milk
• the presence of normal levels of milk protein transcripts in mutant mammary gland suggests that protein translation was perturbed in the mutant tissue

growth/size/body
• a high percentage of homozygous mutant mice failed to control their ear movement: one or sometimes both ears were curled back towards the body
• homozygous mutant mice were viable but showed severe postnatal growth reduction
• adult homozygous mutant males were only about 10% smaller than wild-type mice, whereas females had a 35% lower body weight
• all organs were proportionally smaller in both sexes

hearing/vestibular/ear
• a high percentage of homozygous mutant mice failed to control their ear movement: one or sometimes both ears were curled back towards the body

reproductive system
• most homozygous mutant females were unable to give birth because developing blastocysts failed to implant into the uterine wall

skeleton
• bone formation and mineralization, chondrocyte proliferation, apoptosis, and the morphology of the growth plates in the tibia and metatarsus appeared normal; however, mutants exhibited lack of proper mineralization of the fibula bone and a narrow pelvis

craniofacial
• a high percentage of homozygous mutant mice failed to control their ear movement: one or sometimes both ears were curled back towards the body

integument
• the mammary epithelium of virgin mice was hyperproliferative
• the mutant mammary glands displayed enlarged terminal end buds due to aberrant ductal growth
• the number of secondary ducts was increased, the ducts had wider lumens, and significantly larger amounts of extracellular matrix were deposited around the ducts
• during pregnancy, loss of encoded protein perturbed the lobuloalveolar proliferation and differentiation, resulting in a large number of alveoli that were unable to secrete milk
• the presence of normal levels of milk protein transcripts in mutant mammary gland suggests that protein translation was perturbed in the mutant tissue

cellular
• the mammary epithelium of virgin mice was hyperproliferative


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
07/22/2025
MGI 6.24
The Jackson Laboratory