Analysis Tools|
Allele Symbol Allele Name Allele ID |
Tg(Col2a1-PTHR1*H223R)AHju transgene insertion A, Harald Juppner MGI:3584013 |
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| Summary |
8 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice exhibit normal bone length
• tibial growth plate of mutants is similar to wild-type, indicating rescue of the chondrocyte differentiation delay seen in single Tg(Col2a1-PTHR1*H223R)AHju/0 mice and improvement in endochondral bone formation
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Histological tibiae sections of mice homozygous for Tg(Col2a1-PTHR1*H223R)AHju, mice homozygous for Tg(Col2a1-PTHR1*H223R)AHju and Pthlhtm1Hmk and mice homozygous for Pthlhtm1Hmk
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• survive up to 2 months compared to death around birth in single Pthlh homozygous null mice
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• the odontoblast layer is disorganized
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• number of ameloblasts is reduced
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• tooth eruption is lacking even though tooth buds develop
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• although the endochondral bone formation defect of Pthlh homozygous null mice is rescued, mutant mice are malnourished and grow less than controls
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• the odontoblast layer is disorganized
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• number of ameloblasts is reduced
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• tooth eruption is lacking even though tooth buds develop
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• premature disappearance of the growth plates and their secondary ossification centers
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• the odontoblast layer is disorganized
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• number of ameloblasts is reduced
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• tooth eruption is lacking even though tooth buds develop
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• increase in length of the columnar region compared to Pthlh mutant mice that express the constitutively active PTHR1 but do not overexpress IHH
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Alizarin red S stained skeletal images of hemizygous and homozygous Tg(Col2a1-PTHR1*H223R)AHju and Pthlhtm1Hmk/Pthlhtm1Hmk mice
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• postnatal survival is prolonged for up to 2 months compared to death around birth in single Pthlh homozygous null mice
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| N |
• at birth or before birth, mutant skeletons appear normal and do not exhibit premature or abnormal mineralization, indicating rescue by the transgene
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• growth plate of the distal tibia at E17.5 shows relatively normal appearance except for mild shortening of the columnar region and delayed blood vessel invasion
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• expansion of fully differentiated hypertrophic chondrocytes in tibia
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Skeletal images of wild-type and Tg(Col2a1-PTHR1*H223R)AHju/Tg(Col2a1-PTHR1*H223R)AHju mice
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• ossification centers of vertebrae are reduced in size
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• at birth, show reduced or absent mineralization of many elements that develop by endochondral bone formation such as the supraoccipital bone, sternum, ischium and pubic bone
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• sternebrae of newborns have no blood vessel invasion and almost no hypertrophic chondrocytes and the middle part of tibiae are still occupied by cartilage at E17.5
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Histological sternum sections of wild-type, and mice hemizygous and homozygous for Tg(Col2a1-PTHR1*H223R)AHju
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• decrease in the number of hypertrophic chondrocytes
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• ossification centers of vertebrae are reduced in size, however less pronounced than in homozygous transgenic mice
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• metaphyseal chondrodysplasia
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• at birth, show reduced or absent mineralization of many elements that develop by endochondral bone formation such as the supraoccipital bone, sternum, ischium and pubic bone, however, less pronounced than in homozygous transgenic mice
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• impaired endochondral ossification, with extended growth plate length and absence of a clear secondary ossification center
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• sternebrae of newborns have no blood vessel invasion and the middle part of tibiae are still occupied by cartilage at E17.5, however less pronounced than in homozygous transgenic mice
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• delay in chondrocyte differentiation
• decease in chondrocyte apoptosis
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• expansion of fully differentiated hypertrophic chondrocytes in tibia
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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 11/12/2024 MGI 6.24 |
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