All Phenotypes Ucp2<tm1Rcq> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Ucp2^tm1Rcq/Ucp2^tm1Rcq	involves: 129X1/SvJ * C57BL/6	MGI:3798691
hm2	Ucp2^tm1Rcq/Ucp2^tm1Rcq	involves: 129X1/SvJ * C57BL/6J	MGI:3045174

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

decreased neuron apoptosis ( J:107995 )

• fewer apoptotic cells are detected in contralateral hemisphere 3 days after MCAO, but distribution of TUNEL-labeled cells in striatal border and neocortical border zones of peri-infarct area is similar in wild-type and mutant brains

• cytosolic release of cytochrome C by mitochondria during cell death is largely reduced in mutants compared to wild-type following MCAO-induced ischemia

decreased susceptibility to ischemic brain injury ( J:107995 )

decreased cerebral infarct size ( J:107995 )

• 3 days after focal ischemia induced by permanent middle cerebral artery occlusion (MCAO), infarct volume is significantly reduced compared to wild-type mice

cellular

cellular phenotype ( J:120450 )

• proton leak (basal proton conductance) in mitochondria from liver, spleen, and lung show no difference from wild-type controls

• LPS treatment does not induce differences in proton leak shown by lung mitochondria

• retinoids do not have different effects on respiratory rates between wild-type and mutant mitochondria

• superoxide does not alter mitochondrial respiration in kidneys

decreased cellular sensitivity to oxidative stress ( J:107995 )

• malondialdehyde (MDA) levels are reduced by 30% in mutant brains after MCAO relative to controls, indicating lower oxidative injury

decreased neuron apoptosis ( J:107995 )

• cytosolic release of cytochrome C by mitochondria during cell death is largely reduced in mutants compared to wild-type following MCAO-induced ischemia

abnormal mitochondrial physiology ( J:107995 , J:133277 )

• following lipopolysaccharide treatment, mutant macrophages exhibit only 27% loss of glutathione (GSH) compared to 42% loss in wild-type (J:107995)

• following lipopolysaccharide treatment and GSH addition, macrophages show only a 14% capacity for GSH uptake compared to 80% in wild-type (J:107995)

• in presence of glutamine, macrophages show lower ammonium release, decreased respiratory rate, and intracellular accumulation of aspartate relative to wild-type cells (J:133277)

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:122094 )

N	• circulating triglyceride levels are not different from wild-type

decreased circulating glucose level ( J:122094 )

• levels are significantly lower than in wild-type

decreased circulating lactate level ( J:122094 )

• lactate levels are significantly lower than in wild-type

decreased adiponectin level ( J:122094 )

• levels are significantly lower than in wild-type

decreased susceptibility to ischemic brain injury ( J:107995 )

decreased cerebral infarct size ( J:107995 )

• 3 days after focal ischemia induced by permanent middle cerebral artery occlusion (MCAO), infarct volume is significantly reduced compared to wild-type mice

hematopoietic system

hematopoietic system phenotype ( J:120450 )

N	• no differences in ADP/ATP ratio are observed in spleen

respiratory system

respiratory system phenotype ( J:120450 )

N	• no differences in ADP/ATP ratio are observed in lungs

Allelic Composition	Ucp2^tm1Rcq/Ucp2^tm1Rcq
Genetic Background	involves: 129X1/SvJ * C57BL/6J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ucp2^tm1Rcq mutation (0 available); any Ucp2 mutation (39 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

decreased susceptibility to infection induced morbidity/mortality ( J:66262 )

• wild-type mice displayed a rapid and sustained decline in body weight (<65% of original body weight at death) and succumbed to T. gondii infection within 28-51 days; in contrast, homozygotes displayed prolonged survival and maintained their weight over the 80-day chronic phase of infection

growth/size/body

growth/size/body region phenotype ( J:66262 )

N	• homozygotes were viable, fertile, and of normal appearance and body weight

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:66262 )

N	• homozygotes exhibited a normal response to cold exposure or high-fat diet

immune system

abnormal macrophage physiology ( J:66262 )

• mutant macrophages eliminated T. gondii tachyzoites more efficiently than wild-type

• mutant macrophages showed normal phagocytosis but generated more reactive oxygen species (ROS) than wild-type (80% increase) in response to parasitic infection

• in vitro, mutant macrophages displayed a 5-fold increase in toxoplasmacidal activity relative to wild-type

• addition of an ROS quencher to isolated macrophages blunted their ability to eliminate the parasite

decreased susceptibility to bacterial infection ( J:66262 )

• mutant macrophages challenged with Salmonella typhimurium displayed greater bactericidal activity relative to wild-type