Phenotypes associated with this allele
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trip11tm1.1Psmi mutation
(1 available);
any
Trip11 mutation
(99 available)
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normal phenotype
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• homozygotes for this conditional allele are indistinguishable from wild-type and heterozygous controls
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normal phenotype
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• despite the absence of a gene invovled in vesicle transport, no swelling of the endoplasmic reticulum cisternae is found in the acinar cells of the adult pancreas
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm4(ACTB-tdTomato,-EGFP)Luo mutation
(10 available);
any
Gt(ROSA)26Sor mutation
(944 available)
Tg(VAV1-cre)1Graf mutation
(1 available)
Trip11tm1.1Psmi mutation
(1 available);
any
Trip11 mutation
(99 available)
Trip11tm1.2Psmi mutation
(0 available);
any
Trip11 mutation
(99 available)
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immune system
skeleton
N |
• these mice, which have a hemotopoietic conditional null of a gene involved in vesicle transport, develop normally with both endochondral and intramembranous bones being of normal size and mineralization, the osteoblasts have normal Golgi apparatus stack structure and no swelling of the endoplasmic, the humeri at birth show normal trabeculae, cortical bone, and bone marrow, and micro CT measurements at 6 weeks of age are normal, so osteoblast and osteoclast function appear normal
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|
Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm4(ACTB-tdTomato,-EGFP)Luo mutation
(10 available);
any
Gt(ROSA)26Sor mutation
(944 available)
Tg(BGLAP-cre)1Clem mutation
(1 available)
Trip11tm1.1Psmi mutation
(1 available);
any
Trip11 mutation
(99 available)
Trip11tm1.2Psmi mutation
(0 available);
any
Trip11 mutation
(99 available)
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cellular
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• humeral osteoblasts have no swelling of the endoplasmic reticulum, but do have an abnormal Golgi apparatus stack structure
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skeleton
N |
• despite the osteoblast-specific disruption of a gene invovled in vesicle transport, these mice develop normally with both endochondral and intramembranous bones being of normal size and mineralization, and the osteoblasts having no swelling of the endoplasmic reticulum, although the osteoblast Golgi apparatus stack structure is not normal, and at 6 weeks of age micro CT measurements are normal
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm4(ACTB-tdTomato,-EGFP)Luo mutation
(10 available);
any
Gt(ROSA)26Sor mutation
(944 available)
Tg(Col2a1-cre)1Bhr mutation
(3 available)
Trip11tm1.1Psmi mutation
(1 available);
any
Trip11 mutation
(99 available)
Trip11tm1.2Psmi mutation
(0 available);
any
Trip11 mutation
(99 available)
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craniofacial
cellular
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• loss of Golgi apparatus stacking found in humeral chondrocytes
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respiratory system
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• histology of newborns shows decreased lung alveolar formation relative to controls, which the authors say appears to be secondary to the small ribcage
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skeleton
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• newborn pups have shorter bones in the extremities
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• assessment of chondrocytes in humeri finds swollen chondrocytes in some areas at E15.5 and widespread just after birth, and electron microscopy shows an increase in the size of the endoplasmic reticulum cisternae and disruption of the Golgi stack structure
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• newborn pups have decreased mineralization of the skull and vertebral column relative to controls
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• E15.5 humeri show delayed formation of the primary ossification center
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limbs/digits/tail
mortality/aging
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• although generated at the expected Mendelian frequency, these mice all die shortly after birth with severe chondrodysplasia
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growth/size/body
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm4(ACTB-tdTomato,-EGFP)Luo mutation
(10 available);
any
Gt(ROSA)26Sor mutation
(944 available)
Tg(CAG-cre/Esr1*)5Amc mutation
(9 available)
Trip11tm1.1Psmi mutation
(1 available);
any
Trip11 mutation
(99 available)
Trip11tm1.2Psmi mutation
(0 available);
any
Trip11 mutation
(99 available)
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cellular
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• primary chondrocyte cultures treated with tamoxifen to inactivate the loxP-flanked allele have a change in the protein profile in the proteomes with many of the proteins with altered expression playing a role in membrane trafficking or Golgi/endoplasmic reticulum function, so while chondrocyte secretion continues to function the specific set of secreted proteins differs
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