Phenotypes associated with this allele
|
|
| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rgntm1Aish mutation
(0 available);
any
Rgn mutation
(5 available)
|
|
|
liver/biliary system
 |
• hepatocytes exposed to RNF-alpha and actinomycin D showed a 40% higher level of apoptosis than did cells from wild-type
• caspase-8 activity was doubled
• animals became more susceptible to apoptosis after receiving non-lethal doses of anti-FAS antibody
|
cellular
|
|
• hepatocytes exposed to RNF-alpha and actinomycin D showed a 40% higher level of apoptosis than did cells from wild-type
• caspase-8 activity was doubled
• animals became more susceptible to apoptosis after receiving non-lethal doses of anti-FAS antibody
|
homeostasis/metabolism
vision/eye
|
|
• mice fed a vitamin C-deficient diet and exposed to UVR-B exhibit a greater lens opacity than in controls; location indicates anterior sub-capsular cataract
|
Allelic
Composition |
Rgntm1Aish/Y
|
|
Genetic
Background |
involves: 129P2/OlaHsd |
|
| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rgntm1Aish mutation
(0 available);
any
Rgn mutation
(5 available)
|
|
|
Osteogenic disorder in vitamin C-deficient Rgntm1Aish/Y mice
mortality/aging
 |
• mice fed a vitamin C-deficient diet at 30 days of age die after 37-135 days on the diet
|
|
|
• males show increased mortality rate after 3 months of age, with a mean survival time of about 6 months of age
• mice show atrophy in almost all abdominal organs upon death
|
limbs/digits/tail
|
|
• mice fed a vitamin C-deficient diet beginning at 30 days of age exhibit prominent fracture at the distal end of femurs after 59 days of consuming the diet that is not seen in wild-type mice, indicating the development of scurvy
|
growth/size/body
|
|
• mean body weights of males are about 10%, 15%, and 20% lower than those of wild-type males at 3, 6, and 12 months of age, respectively
|
|
|
• mice fed a vitamin C-deficient diet at 30 days of age start to lose weight after 25-56 days of the diet which is not seen in wild-type mice
(J:108295)
• body weight is lower than wild-type mice at 12 months, but not 6 months, of age
(J:135721)
• exposure to cigarette smoke has no effect on body weight
(J:135721)
|
respiratory system
|
|
• males exhibit enlargement of the peripheral airspace without alveolar destruction at 1, 2, and 6 months of age compared to control males
(J:101810)
• increase in airspace enlargement from 3 to 12 months of age, however no damage or inflammation is seen in the alveoli
(J:135721)
|
|
|
• mice show increased susceptibility to cigarette smoke and develop smoke-induced pulmonary emphysema with marked airspace enlargement and parenchymal destruction
|
cardiovascular system
|
|
• the central vein in livers is enlarged in diameter with aging
|
homeostasis/metabolism
liver/biliary system
|
|
• the central vein in livers is enlarged in diameter with aging
|
|
|
• total hepatic cholesterol level is about 3.3-fold higher than in wild-type livers at 12 months of age
|
|
|
• total hepatic triglyceride level is about 3.5-fold higher than in wild-type livers at 12 months of age
|
|
|
• hepatocytes from 12 month old mutants contain many large and small empty vacuoles (lipid droplets), enlarged mitochondria with indistinct cristae, large lysosomes filled with electron-dense bodies, and absence of well-developed rough-surfaced endoplasmic reticulum, not seen in wild-type hepatocytes
|
|
|
• enlarged mitochondria with indistinct cristae
|
|
|
• livers show an increase in the size and number of lipid droplets with age indicating lipid droplet storage
|
cellular
|
|
• enlarged mitochondria with indistinct cristae
|
|
|
• mice exposed to cigarette smoke for 8 weeks exhibit an increase in protein carbonyls, malondialdehyde, total glutathione and oxidized glutathione in lung cells compared to wild-type mice
• mice exposed to cigarette smoke for 8 weeks exhibit an increase in apoptosis in bronchial and bronchiolar epithelial cells and alveolar septal cells compared to wild-type controls
|
|
|
• 12 month old mice show increased oxidative stress in the brain as indicated by an increase in the generation of reactive species and NADPH oxidase activity, an increase in oxidatively modified proteins, and infiltration of activated leukocytes
(J:107922)
• protein carbonyls are increased in the lungs with age compared to wild-type mice, indicating oxidative stress
(J:135721)
• mice exposed to cigarette smoke for 8 weeks exhibit an increase in protein carbonyls, malondialdehyde, total glutathione and oxidized glutathione, and apoptosis of lung cells compared to wild-type mice, indicating increased susceptibility to oxidative stress induced by smoke exposure
(J:135721)
|
nervous system
|
|
• 12 month old mice show increased oxidative stress in the brain
• brains of 12 months old mice show infiltration of activated leukocytes, however no neuronal loss or damage is seen in the brain
|
adipose tissue
|
|
• mice fed a vitamin C-deficient diet at 30 days of age exhibit a significant decrease in body fat compared to wild-type mice after 59 days of the diet
|
behavior/neurological
|
|
• mice fed a vitamin C-deficient diet at 30 days of age exhibit an abnormal gait after 31-56 days of the diet which is not seen in wild-type mice
|
skeleton
|
|
• mice fed a vitamin C-deficient diet beginning at 30 days of age exhibit prominent fracture at the distal end of femurs after 59 days of consuming the diet that is not seen in wild-type mice, indicating the development of scurvy
|
|
|
• mice fed a vitamin C-deficient diet beginning at 30 days of age exhibit rachitic rosaries at the junction of costae and costal cartilages after 59 days of consuming the diet that is not seen in wild-type mice, indicating the development of scurvy
|
|
|
• mice fed a vitamin C-deficient diet at 30 days of age exhibit a significant decrease in subcranial total bone mineral density compared to wild-type mice after 59 days of the diet
|
integument
|
|
• mice fed a vitamin C-deficient diet beginning at 34 days of age for a total of 36 days exhibit hair follicles in anagen stage compared to wild-type controls which are in telogen stage, however by 60 days of the vitamin C-deficient diet, hair follicles are back in telogen as in controls
|
|
|
• mice fed a vitamin C-deficient diet beginning at 34 days of age for a total of 60 days exhibit a thinner dermis than controls
|
|
|
• mice fed a vitamin C-deficient diet beginning at 34 days of age for a total of 60 days exhibit keratinocytes with flat shapes and many cornified layers remaining on the skin surface compared to wild-type mice
|
Allelic
Composition |
Rgntm1Aish/Y
|
|
Genetic
Background |
involves: 129P2/OlaHsd * C57BL/6 |
|
| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rgntm1Aish mutation
(0 available);
any
Rgn mutation
(5 available)
|
|
|
hearing/vestibular/ear
|
|
• at 10 months of age, mice fed a vitamin-C deficient diet beginning at 30 days of age, exhibit an increase in auditory brainstem response (ABR) thresholds
• mice fed a vitamin-C sufficient diet exhibit normal ABR thresholds
|
homeostasis/metabolism
integument
|
|
• at 10 months of age, mice fed a vitamin-C deficient diet beginning at 30 days of age, exhibit alopecia around the mouth and eyes
|
nervous system
|
|
• at 10 months of age, mice fed a vitamin-C deficient diet beginning at 30 days of age, exhibit a decrease in the number of spiral ganglion cells compared to wild-type mice, indicating degeneration of these cells
• mice fed a vitamin-C sufficient diet exhibit a normal density of spiral ganglion cells
|
vision/eye
|
|
• mice fed a vitamin C-deficient diet and exposed to UVR-B exhibit a greater lens opacity than in controls; location indicates anterior sub-capsular cataract
|
Analysis Tools