Phenotypes associated with this allele

• Allele Symbol: Mt1^tm1Bri
• Allele Name: targeted mutation 1, Ralph L Brinster
• Allele ID: MGI:1857301
• Summary: 9 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cx1	Mt1^tm1Bri/Mt1^tm1Bri Mt2^tm1Bri/Mt2^tm1Bri	129S7/SvEvBrd-Mt1^tm1Bri Mt2^tm1Bri	MGI:3764512
cx2	Mt1^tm1Bri/Mt1^tm1Bri Mt2^tm1Bri/Mt2^tm1Bri	129S7/SvEvBrd-Mt1^tm1Bri Mt2^tm1Bri/J	MGI:4361585
cx3	Mt1^tm1Bri/Mt1^tm1Bri Mt2^tm1Bri/Mt2^tm1Bri	involves: 129S7/SvEvBrd	MGI:4361574
cx4	Atp7a^Mo-brJ/Atp7a^+ Mt1^tm1Bri/Mt1^tm1Bri Mt2^tm1Bri/Mt2^tm1Bri	involves: 129S7/SvEvBrd * C3H/HeJ	MGI:4361578
cx5	Atp7a^Mo-brJ/Y Mt1^tm1Bri/Mt1^tm1Bri Mt2^tm1Bri/Mt2^tm1Bri	involves: 129S7/SvEvBrd * C3H/HeJ * C57BL/6J	MGI:4361577
cx6	Atp7a^Mo-brJ/Atp7a^+ Mt1^tm1Bri/Mt1^tm1Bri Mt2^tm1Bri/Mt2^tm1Bri Tg(Mt1)174Bri/0	involves: 129S7/SvEvBrd * C3H/HeJ * C57BL/6 * SJL	MGI:4361575
cx7	Mt1^tm1Bri/Mt1^tm1Bri Mt2^tm1Bri/Mt2^tm1Bri	involves: 129S7/SvEvBrd * C57BL/6	MGI:3798857
cx8	Mt1^tm1Bri/Mt1^tm1Bri Mt2^tm1Bri/Mt2^tm1Bri	involves: 129S7/SvEvBrd * C57BL/6J	MGI:4361628
cx9	Mt1^tm1Bri/Mt1^tm1Bri Mt2^tm1Bri/Mt2^tm1Bri	involves: 129S7/SvEvBrd * CD-1	MGI:4361592

Genotype
MGI:3764512

cx1

• Allelic Composition: Mt1^tm1Bri/Mt1^tm1Bri; Mt2^tm1Bri/Mt2^tm1Bri
• Genetic Background: 129S7/SvEvBrd-Mt1^tm1Bri Mt2^tm1Bri

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

mortality/aging

premature death ( J:16487 )

• death occurs between 2-4 days after administration of cadmium, no deaths are observed in control mice

• males die earlier and more often than females after cadmium injection

liver/biliary system

abnormal liver morphology ( J:16487 )

• 4 days after administration of cadmium, livers exhibit focal areas of cellular degeneration, necrosis, congestion and hemorrhaging

hepatic necrosis ( J:16487 )

• necrosis observed following administration of cadmium

liver degeneration ( J:16487 )

• degeneration observed following administration of cadmium

homeostasis/metabolism

abnormal circulating enzyme level ( J:16487 )

• untreated females have 2-fold higher levels of serum glutamic-pyruvic transaminase (SGPT) and serum glutamic-oxaloacetic transaminase (SGOT) than untreated controls

• following 2 days of cadmium treatment, males exhibit a significant increase in SGOT and SGPT levels over treated control males

increased circulating alkaline phosphatase level ( J:16487 )

• increased levels observed in untreated males and females as compared to controls

Genotype
MGI:4361585

cx2

• Allelic Composition: Mt1^tm1Bri/Mt1^tm1Bri; Mt2^tm1Bri/Mt2^tm1Bri
• Genetic Background: 129S7/SvEvBrd-Mt1^tm1Bri Mt2^tm1Bri/J

mortality/aging

increased susceptibility to xenobiotic induced morbidity/mortality ( J:120196 )

• nickel-treated mice exhibit reduced mean survival time compared with similarly treated wild-type mice

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:59769 )

N • mice exhibit normal sensitivity to MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) treatment

increased blood urea nitrogen level ( J:126620 )

• in cadmium-treated mice

increased urine glucose level ( J:126620 )

• in cadmium-treated mice

abnormal zinc homeostasis ( J:89429 )

• kainic acid-treated mice exhibit a greater increase in histochemically reactive zinc compared with similarly treated wild-type mice

abnormal physiological response to xenobiotic ( J:56770 , J:126620 )

• 4-hydroxybutyl(butyl)nitrosamine-treated mice develop tumors with less malignant potential than in similarly treated wild-type mice (J:56770)

• treatment with zinc does not alter chemically-induced tumor formation unlike in wild-type mice (J:56770)

• mice treated with high doses of cadmium exhibit decreased renal cadmium and zinc concentrations compared with similarly treated wild-type mice (J:126620)

increased susceptibility to xenobiotic induced morbidity/mortality ( J:120196 )

• nickel-treated mice exhibit reduced mean survival time compared with similarly treated wild-type mice

increased physiological sensitivity to xenobiotic ( J:89429 , J:126420 , J:126620 )

• apoptosis in the hippocampal neurons of kainic acid-treated mice is increased compared to in wild-type mice (J:89429)

• kainic acid-treated mice exhibit fewer GFAP+ astrocytes and lectin+ microglia than in wild-type mice most of which maintain pretreatment morphology (J:89429)

• kainic acid-treated mice exhibit a greater increase in histochemically reactive zinc compared with similarly treated wild-type mice (J:89429)

• cadmium-chloride-treated mice exhibit more loss of weight, bone mass, ash weight, and calcium content at lower doses than similarly treated wild-type mice (J:126420)

• cadmium-chloride-treated mice exhibit a thickening in bony trabecular in the metaphysis, thickening in bony trabecular in the metaphysis, thinning of metaphyseal cortical bone, and dilation of the haversian canals compared with similarly treated wild-type mice (J:126420)

• cadmium-chloride-treated mice exhibit a thinning of the femoral epiphyseal growth plate with expansion of the marrow on either side of the plate and extensive loss of the epiphyseal ossification zone unlike in similarly treated wild-type mice (J:126420)

• mice treated with chronic high doses of cadmium exhibit enlarged kidneys and livers and increased renal injury compared with similarly treated wild-type mice as determined by increased urinary excretion of gamma-GT and glucose, blood urea nitrogen levels, severe proximal convoluted tubule atrophy and cystic dilation, chronic inflammation, interstitial nephritis and fibrosis, extensive necrosis, apoptosis, tubular degeneration, dilated collecting tubules, glomerular swelling, and foci of microcalcification (J:126620)

• however, cadmium-treated mice exhibit normal urinary excretion of protein and NAG (J:126620)

increased incidence of tumors by chemical induction ( J:56770 )

• BBN-treated mice develop more tumors with less malignant potential than similarly treated wild-type mice

increased susceptibility to injury ( J:62369 )

• UVB-treated mice exhibit more sunburn cells and apoptotic cells compared with similarly treated wild-type mice

immune system

enlarged spleen ( J:110643 )

increased spleen weight ( J:110643 )

spleen hyperplasia ( J:110643 )

increased neutrophil cell number ( J:120196 )

• neutrophils are increased in the bronchoalveolar lavage of nickel-treated mice compared to in similarly treated wild-type mice

decreased B cell number ( J:110643 )

• ovalbumin-specific B cells are decreased compared to in wild-type mice

• circulatory B cells are decreased compared to in wild-type mice

• CD19+ B cells in the spleen are decreased 11% compared to in wild-type mice

decreased T cell number ( J:110643 )

• circulating T cells

increased lymphocyte cell number ( J:110643 )

• 20% more than in wild-type mice in the spleen

increased plasma cell number ( J:110643 )

• untreated and ovalbumin-treated mice exhibit increased antibody-secreting plasma cells in the spleen compared with wild-type mice

increased CD4-positive, alpha-beta T cell number ( J:110643 )

• 9% more than in wild-type mice in the spleen

increased CD8-positive, alpha-beta T cell number ( J:110643 )

• 4% more than in wild-type mice in the spleen

abnormal microglial cell morphology ( J:89429 )

• kainic acid-treated mice exhibit fewer lectin+ microglia that maintain pretreatment morphology unlike in similarly treated wild-type mice

abnormal lymphocyte physiology ( J:110643 )

• LPS- and Con A-stimulated lymphocyte proliferation in the spleen is increased compared to in similarly treated wild-type mice

increased thymocyte apoptosis ( J:57169 )

• following gamma-irradiation with 5 Gray, the number of thymocytes undergoing apoptosis is increased compared with similarly treated wild-type mice

• however, treatment with 10 Gray of gamma irradiation induces the same amount of thymocyte apoptosis as in similarly treated wild-type mice

increased IgG level ( J:110643 )

• in ovalbumin-treated mice

increased IgM level ( J:110643 )

• in ovalbumin-treated mice

abnormal humoral immune response ( J:110643 )

• mice exhibit increased humoral response to ovalbumin with increased levels of IgG and IgM compared with similarly treated wild-type mice

kidney inflammation ( J:126620 )

• in cadmium-treated mice

lung inflammation ( J:120196 )

• in nickel-treated mice

renal/urinary system

increased renal tubule apoptosis ( J:126620 )

• in cadmium-treated mice

enlarged kidney ( J:126620 )

• in cadmium-treated mice

increased urine glucose level ( J:126620 )

• in cadmium-treated mice

kidney inflammation ( J:126620 )

• in cadmium-treated mice

dilated kidney collecting duct ( J:126620 )

• in cadmium-treated mice

renal interstitial fibrosis ( J:126620 )

• in cadmium-treated mice

kidney atrophy ( J:126620 )

• severe proximal convoluted tubule atrophy in cadmium-treated mice

dilated proximal convoluted tubule ( J:126620 )

• cystic dilation in cadmium-treated mice

kidney degeneration ( J:126620 )

• tubular degeneration in cadmium-treated mice

nephrocalcinosis ( J:126620 )

• foci of microcalcification in cadmium-treated mice

renal necrosis ( J:126620 )

• extensive necrosis in cadmium-treated mice

nervous system

increased susceptibility to pharmacologically induced seizures ( J:89429 )

• mice exhibit increased number, frequency, and duration of kainic acid-induced limb clonus and tonic-clonic convulsions compared with similarly treated wild-type mice

clonic seizures ( J:89429 )

• mice exhibit increased number, frequency, and duration of kainic acid-induced limb clonus and tonic-clonic convulsions compared with similarly treated wild-type mice

tonic-clonic seizures ( J:89429 )

• mice exhibit increased number, frequency, and duration of kainic acid-induced limb clonus and tonic-clonic convulsions compared with similarly treated wild-type mice

increased neuron apoptosis ( J:89429 )

• apoptosis in the hippocampal neurons of kainic acid-treated mice is increased compared to in wild-type mice

abnormal microglial cell morphology ( J:89429 )

• kainic acid-treated mice exhibit fewer lectin+ microglia that maintain pretreatment morphology unlike in similarly treated wild-type mice

abnormal astrocyte morphology ( J:89429 )

• mice have fewer GFAP+ astrocytes compared with wild-type mice

• kainic acid-treated mice exhibit fewer GFAP+ astrocytes than in wild-type mice, most of which maintain pretreatment morphology

behavior/neurological

increased susceptibility to pharmacologically induced seizures ( J:89429 )

• mice exhibit increased number, frequency, and duration of kainic acid-induced limb clonus and tonic-clonic convulsions compared with similarly treated wild-type mice

abnormal learning/memory/conditioning ( J:112813 )

• in a radial-arm maze, young mice exhibit lower average choice accuracy, reduced improvement in average choice accuracy, and increased response latencies during the acquisition period compared with wild-type mice

• in a radial-arm maze, nicotine-treated young male mice fail to exhibit an improvement in choice accuracy unlike similarly treated wild-type mice

• in a radial-arm maze, aged mice exhibit lower choice accuracy and increased latency compared with wild-type mice

• however, treatment of aged mice in a radial-arm maze with nicotine attenuates their choice accuracy and latency deficits

clonic seizures ( J:89429 )

• mice exhibit increased number, frequency, and duration of kainic acid-induced limb clonus and tonic-clonic convulsions compared with similarly treated wild-type mice

tonic-clonic seizures ( J:89429 )

• mice exhibit increased number, frequency, and duration of kainic acid-induced limb clonus and tonic-clonic convulsions compared with similarly treated wild-type mice

hematopoietic system

enlarged spleen ( J:110643 )

increased spleen weight ( J:110643 )

spleen hyperplasia ( J:110643 )

increased neutrophil cell number ( J:120196 )

• neutrophils are increased in the bronchoalveolar lavage of nickel-treated mice compared to in similarly treated wild-type mice

decreased B cell number ( J:110643 )

• ovalbumin-specific B cells are decreased compared to in wild-type mice

• circulatory B cells are decreased compared to in wild-type mice

• CD19+ B cells in the spleen are decreased 11% compared to in wild-type mice

decreased T cell number ( J:110643 )

• circulating T cells

increased lymphocyte cell number ( J:110643 )

• 20% more than in wild-type mice in the spleen

increased plasma cell number ( J:110643 )

• untreated and ovalbumin-treated mice exhibit increased antibody-secreting plasma cells in the spleen compared with wild-type mice

increased CD4-positive, alpha-beta T cell number ( J:110643 )

• 9% more than in wild-type mice in the spleen

increased CD8-positive, alpha-beta T cell number ( J:110643 )

• 4% more than in wild-type mice in the spleen

abnormal microglial cell morphology ( J:89429 )

• kainic acid-treated mice exhibit fewer lectin+ microglia that maintain pretreatment morphology unlike in similarly treated wild-type mice

abnormal lymphocyte physiology ( J:110643 )

• LPS- and Con A-stimulated lymphocyte proliferation in the spleen is increased compared to in similarly treated wild-type mice

increased thymocyte apoptosis ( J:57169 )

• following gamma-irradiation with 5 Gray, the number of thymocytes undergoing apoptosis is increased compared with similarly treated wild-type mice

• however, treatment with 10 Gray of gamma irradiation induces the same amount of thymocyte apoptosis as in similarly treated wild-type mice

increased IgG level ( J:110643 )

• in ovalbumin-treated mice

increased IgM level ( J:110643 )

• in ovalbumin-treated mice

skeleton

abnormal long bone epiphyseal plate morphology ( J:126420 )

• cadmium-chloride-treated mice exhibit a thinning of the femoral epiphyseal growth plate with expansion of the marrow on either side of the plate unlike in similarly treated wild-type mice

abnormal long bone epiphyseal ossification zone morphology ( J:126420 )

• extensively lost in cadmium-chloride-treated mice

decreased bone mineral content ( J:126420 )

• cadmium-chloride-treated mice exhibit more loss of bone calcium content than similarly treated wild-type mice

abnormal compact bone morphology ( J:126420 )

• cadmium-chloride-treated mice exhibit dilation of the haversian canals with increased osteoid seams and rounded osteocytes compared with similarly treated wild-type mice

decreased compact bone thickness ( J:126420 )

• cadmium-chloride-treated mice exhibit thinning of metaphyseal cortical bone

abnormal trabecular bone morphology ( J:126420 )

• cadmium-chloride-treated mice exhibit a thickening in bony trabecular in the metaphysis compared with similarly treated wild-type mice

decreased bone mass ( J:126420 )

• cadmium-chloride-treated mice exhibit more loss of bone mass at lower doses than similarly treated wild-type mice

neoplasm

increased incidence of tumors by chemical induction ( J:56770 )

• BBN-treated mice develop more tumors with less malignant potential than similarly treated wild-type mice

liver/biliary system

decreased hepatocyte proliferation ( J:109814 )

• following partial hepatectomy compared to in similarly treated wild-type mice

enlarged liver ( J:126620 )

• in cadmium-treated mice

impaired liver regeneration ( J:109814 )

• hepatocyte proliferation following partial hepatectomy is decreased compared to in similarly treated wild-type mice

growth/size/body

weight loss ( J:126420 )

enlarged kidney ( J:126620 )

• in cadmium-treated mice

enlarged liver ( J:126620 )

• in cadmium-treated mice

enlarged spleen ( J:110643 )

increased spleen weight ( J:110643 )

spleen hyperplasia ( J:110643 )

reproductive system

abnormal reproductive system physiology ( J:103039 )

• mice exhibit poor reproductive success due to high spontaneous embryo resorption ratio

respiratory system

lung inflammation ( J:120196 )

• in nickel-treated mice

cellular

increased thymocyte apoptosis ( J:57169 )

• following gamma-irradiation with 5 Gray, the number of thymocytes undergoing apoptosis is increased compared with similarly treated wild-type mice

• however, treatment with 10 Gray of gamma irradiation induces the same amount of thymocyte apoptosis as in similarly treated wild-type mice

increased renal tubule apoptosis ( J:126620 )

• in cadmium-treated mice

increased neuron apoptosis ( J:89429 )

• apoptosis in the hippocampal neurons of kainic acid-treated mice is increased compared to in wild-type mice

decreased hepatocyte proliferation ( J:109814 )

• following partial hepatectomy compared to in similarly treated wild-type mice

endocrine/exocrine glands

increased thymocyte apoptosis ( J:57169 )

• following gamma-irradiation with 5 Gray, the number of thymocytes undergoing apoptosis is increased compared with similarly treated wild-type mice

• however, treatment with 10 Gray of gamma irradiation induces the same amount of thymocyte apoptosis as in similarly treated wild-type mice

Genotype
MGI:4361574

cx3

• Allelic Composition: Mt1^tm1Bri/Mt1^tm1Bri; Mt2^tm1Bri/Mt2^tm1Bri
• Genetic Background: involves: 129S7/SvEvBrd

mortality/aging

increased susceptibility to xenobiotic induced morbidity/mortality ( J:120459 )

• mice are more sensitive to acetaminophen-induced lethality compared with similarly treated wild-type mice

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:33276 )

N • mice exhibit normal copper levels

increased circulating alanine transaminase level ( J:120459 )

• in acetaminophen-treated mice

abnormal lipid homeostasis ( J:120459 )

• acetaminophen-induced lipid peroxidation is increased compared to in similarly treated wild-type mice

abnormal zinc homeostasis ( J:34407 )

• neonates exhibit a 60% decrease in hepatic zinc levels compared to in wild-type mice

• at 3 weeks, mice from dams fed a low zinc diet exhibit persistently low kidney and bone zinc levels

• however, kidney zinc levels in neonates are normal

• following administration of zinc, mice exhibit a 100% less zinc accumulation in the liver and pancreas compared with similarly treated wild-type mice

abnormal liver zinc level ( J:34407 )

• neonates exhibit a 60% decrease in hepatic zinc levels compared to in wild-type mice

• following administration of zinc, mice exhibit a 100% less zinc accumulation in liver compared with similarly treated wild-type mice

increased susceptibility to xenobiotic induced morbidity/mortality ( J:120459 )

• mice are more sensitive to acetaminophen-induced lethality compared with similarly treated wild-type mice

increased physiological sensitivity to xenobiotic ( J:120459 )

• mice exhibit increased susceptibility to acetaminophen-induced hepatotoxicity, alanine aminotransferase, hepatic necrosis, lipid peroxidation, and lethality compared with similarly treated wild-type mice

• acetaminophen-induced injuries are not ameliorated by pretreatment with zinc unlike in similarly treated wild-type mice

• hepatocytes are more sensitive to acetaminophen and NAPQI-induced oxidative stress compared with similarly treated wild-type cells

• however, acetaminophen metabolism is normal

impaired wound healing ( J:53929 )

• following brain freeze injury, tissue damage is greater than in wild-type mice with increased microglia/macrophage accumulation around the lesion, different temporal microglial response, increased astrocytosis, and increased apoptosis in the brain

• 10 to 20 days post brain freeze injury, mice develop hemorrhage unlike similarly treated wild-type mice

renal/urinary system

increased glomerular capsule space ( J:34407 )

• regardless of diet zinc content, Bowman's spaces are swollen unlike in wild-type mice

abnormal renal glomerulus morphology ( J:34407 )

• unlike in wild-type mice, glomeruli remain close to the kidney capsule in mature kidneys at 3 weeks

• mice fed a low zinc diet exhibit a persistence of the glomeruli remaining close to the kidney unlike in similarly treated wild-type mice

• however, mice fed a normal diet exhibit normal kidney morphology

liver/biliary system

abnormal liver zinc level ( J:34407 )

• neonates exhibit a 60% decrease in hepatic zinc levels compared to in wild-type mice

• following administration of zinc, mice exhibit a 100% less zinc accumulation in liver compared with similarly treated wild-type mice

abnormal hepatocyte morphology ( J:120459 )

• hepatocytes are more sensitive to acetaminophen and NAPQI-induced oxidative stress indicated by lactate dehydrogenase leakage compared with similarly treated wild-type cells

hepatic necrosis ( J:120459 )

• in acetaminophen-treated mice

endocrine/exocrine glands

abnormal pancreas morphology ( J:34407 )

• when administered zinc, 4 of 6 mice exhibit abnormal pancreas morphology with acinar cell necrosis and fibrosis compared to 1 of 6 wild-type mice

cellular

increased sensitivity to induced cell death ( J:33276 )

• cells from E11 embryos exhibit increased cell death when cultured with copper compared with similarly treated heterozygous cells

increased neuron apoptosis ( J:103102 )

• in MOG-treated mice

increased brain apoptosis ( J:53929 )

• 10 and 20 days following brain freeze injury, mice exhibit more apoptosis in the brain compared with similarly treated wild-type mice

oxidative stress ( J:103102 )

• MOG-treated mice exhibit increased oxidative stress in microglia/macrophages and neurons compared with similarly treated wild-type mice

cardiovascular system

hemorrhage ( J:53929 )

• 10 to 20 days post brain freeze injury, mice develop hemorrhage unlike similarly treated wild-type mice

hematopoietic system

increased macrophage cell number ( J:53929 )

• following brain freeze injury, mice exhibit increased microglia/macrophage accumulation around the lesion compared with similarly treated wild-type mice

abnormal microglial cell morphology ( J:53929 , J:103102 )

• following brain freeze injury, mice exhibit increased microglia/macrophage accumulation around the lesion compared with similarly treated wild-type mice (J:53929)

• MOG-treated mice exhibit amoeboid or round microglia/macrophages compared to bushy microglia observed in similarly treated wild-type mice (J:103102)

abnormal microglial cell physiology ( J:53929 )

• microglial temporal response to brain freeze injury is different than in similarly treated wild-type mice

immune system

increased macrophage cell number ( J:53929 )

• following brain freeze injury, mice exhibit increased microglia/macrophage accumulation around the lesion compared with similarly treated wild-type mice

abnormal microglial cell morphology ( J:53929 , J:103102 )

• following brain freeze injury, mice exhibit increased microglia/macrophage accumulation around the lesion compared with similarly treated wild-type mice (J:53929)

• MOG-treated mice exhibit amoeboid or round microglia/macrophages compared to bushy microglia observed in similarly treated wild-type mice (J:103102)

abnormal microglial cell physiology ( J:53929 )

• microglial temporal response to brain freeze injury is different than in similarly treated wild-type mice

increased interleukin-1 beta secretion ( J:103102 )

• MOG-treated mice exhibit increased IL1b production in the brain stem compared with similarly treated wild-type mice

increased interleukin-6 secretion ( J:103102 )

• MOG-treated mice exhibit increased IL6 production in the brain stem compared with similarly treated wild-type mice

increased tumor necrosis factor secretion ( J:103102 )

• MOG-treated mice exhibit increased TNF-alpha production in the brain stem compared with similarly treated wild-type mice

increased susceptibility to experimental autoimmune encephalomyelitis ( J:103102 )

• MOG-treated mice exhibit increased incidence of experimental autoimmune encephalomyelitis, increased inflammatory infiltrate including amoeboid or round microglia/macrophages, and CD3+ T cells, decreased reactive astrogliosis, increased production of IL1beta, IL6 and TNF-alpha in the brain stem, increased oxidative stress, and increased neuron and astrocytic apoptosis compared with similarly treated wild-type mice

nervous system

increased neuron apoptosis ( J:103102 )

• in MOG-treated mice

increased brain apoptosis ( J:53929 )

• 10 and 20 days following brain freeze injury, mice exhibit more apoptosis in the brain compared with similarly treated wild-type mice

abnormal microglial cell morphology ( J:53929 , J:103102 )

• following brain freeze injury, mice exhibit increased microglia/macrophage accumulation around the lesion compared with similarly treated wild-type mice (J:53929)

• MOG-treated mice exhibit amoeboid or round microglia/macrophages compared to bushy microglia observed in similarly treated wild-type mice (J:103102)

abnormal microglial cell physiology ( J:53929 )

• microglial temporal response to brain freeze injury is different than in similarly treated wild-type mice

astrocytosis ( J:53929 , J:103102 )

• freeze-injury mice continue to exhibit reactive astrogliosis 20 days post lesion unlike similarly treated wild-type mice (J:53929)

• decreased in MOG-treated mice (J:103102)

Genotype
MGI:4361578

cx4

• Allelic Composition: Atp7a^Mo-brJ/Atp7a⁺; Mt1^tm1Bri/Mt1^tm1Bri; Mt2^tm1Bri/Mt2^tm1Bri
• Genetic Background: involves: 129S7/SvEvBrd * C3H/HeJ

mortality/aging

embryonic lethality, complete penetrance ( J:33276 )

♀ • no mice are recovered at E11

cellular

increased sensitivity to induced cell death ( J:33276 )

♀ • cells from E11 embryos exhibit increased cell death when cultured with copper compared with similarly treated heterozygous cells

growth/size/body

decreased body size ( J:33276 )

♀ • the one surviving mouse was runted

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:33276 )

♀N • the one recovered mouse had normal copper levels in the intestine and liver

Genotype
MGI:4361577

cx5

• Allelic Composition: Atp7a^Mo-brJ/Y; Mt1^tm1Bri/Mt1^tm1Bri; Mt2^tm1Bri/Mt2^tm1Bri
• Genetic Background: involves: 129S7/SvEvBrd * C3H/HeJ * C57BL/6J

mortality/aging

postnatal lethality, complete penetrance ( J:33276 )

♂ • no mice are recovered at P9

embryonic lethality during organogenesis, incomplete penetrance ( J:33276 )

♂ • only one mouse was recovered at E11

cellular

increased sensitivity to induced cell death ( J:33276 )

♂ • cells from E11 embryos exhibit increased cell death when cultured with copper compared with similarly treated heterozygous cells

Genotype
MGI:4361575

cx6

• Allelic Composition: Atp7a^Mo-brJ/Atp7a⁺; Mt1^tm1Bri/Mt1^tm1Bri; Mt2^tm1Bri/Mt2^tm1Bri; Tg(Mt1)174Bri/0
• Genetic Background: involves: 129S7/SvEvBrd * C3H/HeJ * C57BL/6 * SJL

normal phenotype

no abnormal phenotype detected ( J:33276 )

♀ • mice are phenotypically normal

Genotype
MGI:3798857

cx7

• Allelic Composition: Mt1^tm1Bri/Mt1^tm1Bri; Mt2^tm1Bri/Mt2^tm1Bri
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6

digestive/alimentary system

abnormal intestinal mineral absorption ( J:47419 )

• 2 hours after oral dosing with zinc, mice have about a 2-fold higher zinc concentration in the blood than in control mice

Genotype
MGI:4361628

cx8

• Allelic Composition: Mt1^tm1Bri/Mt1^tm1Bri; Mt2^tm1Bri/Mt2^tm1Bri
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6J

homeostasis/metabolism

increased physiological sensitivity to xenobiotic ( J:116275 )

• NMDA-treated mice exhibit reduced cells in the retinal ganglion cell layer compared with similarly treated wild-type mice

• mice fail to exhibit protective effect of ZnSO4 against NMDA-induced retinal ganglion cell layer damage unlike similarly treated wild-type mice

• however, inner plexiform layer thickness following treatment with NMDA is normal

vision/eye

abnormal retina ganglion layer morphology ( J:116275 )

• NMDA-treated mice exhibit reduced cells in the retinal ganglion cell layer compared with similarly treated wild-type mice

Genotype
MGI:4361592

cx9

• Allelic Composition: Mt1^tm1Bri/Mt1^tm1Bri; Mt2^tm1Bri/Mt2^tm1Bri
• Genetic Background: involves: 129S7/SvEvBrd * CD-1

homeostasis/metabolism

abnormal zinc homeostasis ( J:103039 )

• the teratogenic and embryotoxic effects of zinc deficiency are exacerbated compared to in similarly treated wild-type mice