Phenotypes associated with this allele

• Allele Symbol: Tlr2^tm1Kir
• Allele Name: targeted mutation 1, Carsten J Kirschning
• Allele ID: MGI:2674036
• Summary: 11 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Tlr2^tm1Kir/Tlr2^tm1Kir	B6.129-Tlr2^tm1Kir	MGI:3706987
hm2	Tlr2^tm1Kir/Tlr2^tm1Kir	C.129(B6)-Tlr2^tm1Kir/Tvg	MGI:7764765
hm3	Tlr2^tm1Kir/Tlr2^tm1Kir	either: (involves: 129/Sv * C57BL/6) or (involves: 129/Sv * C57BL/6 * C57BL/6J)	MGI:2674040
hm4	Tlr2^tm1Kir/Tlr2^tm1Kir	involves: 129	MGI:4452598
hm5	Tlr2^tm1Kir/Tlr2^tm1Kir	involves: 129 * C57BL/6	MGI:5428445
hm6	Tlr2^tm1Kir/Tlr2^tm1Kir	Not Specified	MGI:3574656
cx7	Ldlr^tm1Her/Ldlr^tm1Her Tlr2^tm1Kir/Tlr2^tm1Kir	B6.129-Tlr2^tm1Kir Ldlr^tm1Her	MGI:5428446
cx8	Tlr2^tm1Kir/Tlr2^tm1Kir Tlr4^tm1Aki/Tlr4^tm1Aki	B6.129-Tlr2^tm1Kir Tlr4^tm1Aki	MGI:3706993
cx9	Tlr2^tm1Kir/Tlr2^tm1Kir Tlr4^Lps-d/Tlr4^Lps-d	C3.Cg-Tlr2^tm1Kir Tlr4^Lps-d	MGI:3706988
cx10	Tlr2^tm1Kir/Tlr2^tm1Kir Tlr4^Lps-d/Tlr4^Lps-d	C.Cg-Tlr2^tm1Kir Tlr4^Lps-d	MGI:7764767
cx11	Tlr2^tm1Kir/Tlr2^tm1Kir Tg(APP695)3Dbo/? Tg(PSEN1)5Dbo/?	involves: 129 * C3H/HeJ * C57BL/6	MGI:5428447

Genotype
MGI:3706987

hm1

• Allelic Composition: Tlr2^tm1Kir/Tlr2^tm1Kir
• Genetic Background: B6.129-Tlr2^tm1Kir

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

mortality/aging

decreased susceptibility to bacterial infection induced morbidity/mortality ( J:121930 )

• mutants are protected from bacterial lipoteichoic acid exposure after priming by IFNG and sensitization with D-galactosamine, while Tlr4-deficient mice and wild-type are susceptible to lethal shock by this treatment

• however, similar to wild-type mice heat-inactivated E. coli exposure results in fatal toxemia

• susceptibilities to L. monocytogenes and S. aureus challenge are not different from wild-type mice

premature death ( J:128329 , J:165105 )

• 60% mortality due to weight loss resulting from induced colonic inflammation (J:128329)

immune system

abnormal cellular extravasation ( J:171028 )

• accumulation of monocyte/macrophage in surrounding tissues is significantly reduced relative to controls after femoral artery ligation

decreased splenocyte proliferation ( J:121930 )

• splenocytes do not proliferate in response to bacterial peptidoglycan or lipoteichoic acid, but do respond normally with proliferation to enterobacterial LPS

increased susceptibility to induced colitis ( J:165105 )

• inflammation level significantly greater 14 days into procedure to induce colitis

decreased circulating tumor necrosis factor level ( J:162168 )

♀ • in females on high fat diet at 20 weeks

♀ • also reduced MCP-1 levels in females on high fat diet at 20 weeks

abnormal cytokine secretion ( J:121930 )

• systemic challenge with Pam3-CSK4, a bacterial lipopeptide analog, does not induce substantial secretion of Il6 or TNFalpha, compared to marked levels produced in wild-type mice

decreased interleukin-1 beta secretion ( J:129871 )

• IL1-beta secretion by peritoneal macrophages is reduced by 50% in response to Listeria infection

• peritoneal macrophages fail to secrete IL-1beta in response to a TLR2 agonist

decreased interleukin-6 secretion ( J:129871 )

• IL-6 secretion by peritoneal macrophages is reduced by 8-fold in response to Listeria infection

• peritoneal macrophages fail to secrete IL6 in response to a TLR2 agonist

decreased tumor necrosis factor secretion ( J:129871 )

• TNF secretion by peritoneal macrophages is reduced by 50% in response to Listeria infection

decreased susceptibility to bacterial infection induced morbidity/mortality ( J:121930 )

• mutants are protected from bacterial lipoteichoic acid exposure after priming by IFNG and sensitization with D-galactosamine, while Tlr4-deficient mice and wild-type are susceptible to lethal shock by this treatment

• however, similar to wild-type mice heat-inactivated E. coli exposure results in fatal toxemia

• susceptibilities to L. monocytogenes and S. aureus challenge are not different from wild-type mice

cellular

increased adipocyte glucose uptake ( J:162168 )

♀ • improved insulin stimulated glucose uptake in females on a high fat diet

decreased neuron apoptosis ( J:124100 )

• neurons are resistant to apoptosis caused by glucose deficiency

abnormal cellular extravasation ( J:171028 )

• accumulation of monocyte/macrophage in surrounding tissues is significantly reduced relative to controls after femoral artery ligation

decreased splenocyte proliferation ( J:121930 )

• splenocytes do not proliferate in response to bacterial peptidoglycan or lipoteichoic acid, but do respond normally with proliferation to enterobacterial LPS

nervous system

decreased neuron apoptosis ( J:124100 )

• neurons are resistant to apoptosis caused by glucose deficiency

decreased cerebral infarct size ( J:124100 )

• damage due to middle cerebral artery occlusion is considerably reduced

brain ischemia ( J:148091 )

• increased mortality occurring within 24 hours due to ischemia/reperfusion

• reduced neurological score after ischemia/reperfusion

• increased infarct size at 24 hours after ischemia/reperfusion

• large areas of pan-necrosis in the distribution area of the middle cerebral artery

homeostasis/metabolism

decreased circulating leptin level ( J:162168 )

♀ • in females on a high fat diet at 20 weeks

decreased circulating tumor necrosis factor level ( J:162168 )

♀ • in females on high fat diet at 20 weeks

♀ • also reduced MCP-1 levels in females on high fat diet at 20 weeks

increased energy expenditure ( J:162168 )

♀ • in females on high fat diet

♀ • preferential use of lipids as an energy source

abnormal glucose homeostasis ( J:162168 )

increased insulin secretion ( J:162168 )

♀ • beta cell insulin secretion in response to glucose challenge is markedly improved in females relative to controls at 20 weeks

decreased circulating insulin level ( J:162168 )

• fasting circulating insulin levels are reduced at both 12 and 20 weeks on a high fat diet

improved glucose tolerance ( J:162168 )

♀ • improved glucose tolerance in females after 12 weeks on a high fat diet relative to controls

♀ • glucose homeostasis on a normal diet is similar to controls

increased insulin sensitivity ( J:162168 )

• insulin sensitivity in response to glucose challenge is markedly improved in females relative to controls at 20 weeks

• liver insulin sensitivity is preserved after 20 weeks on a high fat diet

• reduced hepatic glucose production in a hyperinsulinaemic clamp

• males also show increased insulin sensitivity

decreased cerebral infarct size ( J:124100 )

• damage due to middle cerebral artery occlusion is considerably reduced

decreased susceptibility to kidney reperfusion injury ( J:146120 )

• significantly protected from ischemia reperfusion injury as measured by serum creatinine levels 24 hours after injury

adipose tissue

decreased fat cell size ( J:162168 )

♀ • adipocytes are smaller in females on a high fat diet

decreased gonadal fat pad weight ( J:162168 )

♀ • reduced perigonadal fat pad weight in females on a high fat diet

increased adipocyte glucose uptake ( J:162168 )

♀ • improved insulin stimulated glucose uptake in females on a high fat diet

behavior/neurological

increased food intake ( J:162168 )

♀ • increased calorie consumption in females on a high fat diet

liver/biliary system

decreased susceptibility to hepatic steatosis ( J:162168 )

• reduced lipid content of the liver

cardiovascular system

decreased angiogenesis ( J:171028 )

• perfusion restoration is significantly reduced 7 days after femoral artery ligation

rectal hemorrhage ( J:128329 , J:165105 )

• gross rectal bleeding 5 days after induction of colonic inflammation with dextran sodium sulfate (J:128329)

digestive/alimentary system

rectal hemorrhage ( J:128329 , J:165105 )

• gross rectal bleeding 5 days after induction of colonic inflammation with dextran sodium sulfate (J:128329)

abnormal intestinal epithelium morphology ( J:165105 )

• reduced proliferation and increased apoptosis before experimental manipulation

abnormal enterocyte morphology ( J:128329 )

• compromised intestinal epithelial tight junction barrier

• increased number of apoptotic intestinal epithelial cells

abnormal large intestine crypts of Lieberkuhn morphology ( J:165105 )

• aberrant (preneoplastic) crypt foci

• reduced apoptosis

colonic necrosis ( J:165105 )

• less necrosis in colon than for controls 14 days after beginning procedure to induce colitis

increased gastrointestinal tumor incidence ( J:165105 )

• tumor burden 2X that of controls

• particularly in the proximal colon

• more large tumors

increased colon adenoma incidence ( J:165105 )

• colorectal adenomas with very distorted glands and an increased level of disorganization

increased susceptibility to induced colitis ( J:165105 )

• inflammation level significantly greater 14 days into procedure to induce colitis

growth/size/body

weight loss ( J:128329 , J:165105 )

• severe weight loss as a result of induced colonic inflammation (J:128329)

renal/urinary system

decreased susceptibility to kidney reperfusion injury ( J:146120 )

• significantly protected from ischemia reperfusion injury as measured by serum creatinine levels 24 hours after injury

neoplasm

increased gastrointestinal tumor incidence ( J:165105 )

• tumor burden 2X that of controls

• particularly in the proximal colon

• more large tumors

increased colon adenoma incidence ( J:165105 )

• colorectal adenomas with very distorted glands and an increased level of disorganization

increased carcinoma incidence ( J:165105 )

• two fold increase in the incidence of carcinomas

endocrine/exocrine glands

abnormal large intestine crypts of Lieberkuhn morphology ( J:165105 )

• aberrant (preneoplastic) crypt foci

• reduced apoptosis

increased insulin secretion ( J:162168 )

♀ • beta cell insulin secretion in response to glucose challenge is markedly improved in females relative to controls at 20 weeks

hematopoietic system

abnormal cellular extravasation ( J:171028 )

• accumulation of monocyte/macrophage in surrounding tissues is significantly reduced relative to controls after femoral artery ligation

decreased splenocyte proliferation ( J:121930 )

• splenocytes do not proliferate in response to bacterial peptidoglycan or lipoteichoic acid, but do respond normally with proliferation to enterobacterial LPS

Genotype
MGI:7764765

hm2

• Allelic Composition: Tlr2^tm1Kir/Tlr2^tm1Kir
• Genetic Background: C.129(B6)-Tlr2^tm1Kir/Tvg

neoplasm

neoplasm ( J:329456 )

N • specific-pathogen free (SPF) offspring from mice infected with Rauscher-like murine leukemia virus (MuLV infected offspring) exhibit leukemia latency and incidence similar to wild-type specific-pathogen free mice

Genotype
MGI:2674040

hm3

• Allelic Composition: Tlr2^tm1Kir/Tlr2^tm1Kir
• Genetic Background: either: (involves: 129/Sv * C57BL/6) or (involves: 129/Sv * C57BL/6 * C57BL/6J)

immune system

decreased interleukin-10 secretion ( J:85323 )

• IL-10 secretion by mutant bone marrow-derived macrophages (BMDMs) is abolished in response to 500 ng/ml of B. burgdorferi recombinant outer surface protein A (OspA)

• IL-10 secretion by mutant BMDMs is severely reduced in response to 5 ug/ml of B. burgdorferi OspA

decreased interleukin-6 secretion ( J:85323 )

• IL-6 secretion by mutant BMDMs is abolished in response to 500 ng/ml of B. burgdorferi OspA

• IL-6 secretion by mutant BMDMs is severely reduced in response to 5 ug/ml of B. burgdorferi OspA

abnormal innate immunity ( J:85323 )

• homozygotes exhibit an abnormal innate host defense to infection with Borrelia burgdorferi, as shown by a failure to control spirochete levels in infected tissues

• in contrast, homozygotes develop normal Borrelia-specific Ab responses, indicating that acquired host defense is unimpaired

abnormal macrophage physiology ( J:85323 )

• in vitro, mutant BMDMs do not respond to 500 ng/ml of B. burgdorferi recombinant OspA, as shown by a failure to elicit IL-6, IL-10, TNF and nitrate production relative to BMDMs from control C3H/HeN and C57BL/6 mice

• mutant BMDMs fail to respond to 5 um/ml OspA (a 10-fold higher concentration), as shown by a severely diminished production of nitrate, IL-6, IL-10, and TNF relative to wild-type BMDMs

• mutant BMDMs do respond to nonlipoprotein components of sonicated B. burgdorferi (N40) spirochetes, but require 10- to 100-fold more sonicate for equivalent nitrate production as wild-type BMDMs

• however, mutant BMDMs do show a strong response to repurified LPS (100 ng/ml)

decreased macrophage cytokine production ( J:85323 )

• TNF secretion by mutant BMDMs is abolished in response to 500 ng/ml of B. burgdorferi OspA

• TNF secretion by mutant BMDMs is severely reduced in response to 5 ug/ml of B. burgdorferi OspA

decreased macrophage nitric oxide production ( J:85323 )

• NO production by mutant BMDMs is abolished in response to 500 ng/ml of B. burgdorferi OspA

• NO production by mutant BMDMs is severely reduced in response to 5 ug/ml of B. burgdorferi OspA

• mutant BMDMs do respond to nonlipoprotein components of sonicated B. burgdorferi (N40) spirochetes, but require 10- to 100-fold more sonicate for equivalent nitrate production as wild-type BMDMs

increased susceptibility to bacterial infection ( J:85323 )

• at 4 weeks postinfection with 2 x 10³ organisms of B. burgdorferi (N40 isolate), homozygotes exhibit a striking increase in rear ankle swelling relative to wild-type and heterozygous controls, with both rear ankle joints showing uniformly increased edema; however, individual disease parameters and overall arthritic lesion severity is not significantly different between similarly-infected mutant and control mice

• at 2 and 4 weeks postinfection, all homozygotes harbor up to 100-fold more B. burgdorferi spirochetes in heart, rear ankle joints, and ears than wild-type and heterozygous controls

• at 2 weeks postinfection, homozygotes harbor up ~7-fold more B. burgdorferi spirochetes in spleen than wild-type controls

• in homozygotes, extremely high spirochete levels of B. burgdorferi persist in infected hearts, rear ankles, and ears at 8 weeks postinfection

• however, homozygotes display a normal acquired humoral response to B. burgdorferi infection, as measured by quantity of Borrelia-specific Ig isotypes, the kinetics of class switching to IgG, and the complexity of the antigens recognized

homeostasis/metabolism

decreased macrophage nitric oxide production ( J:85323 )

• NO production by mutant BMDMs is abolished in response to 500 ng/ml of B. burgdorferi OspA

• NO production by mutant BMDMs is severely reduced in response to 5 ug/ml of B. burgdorferi OspA

• mutant BMDMs do respond to nonlipoprotein components of sonicated B. burgdorferi (N40) spirochetes, but require 10- to 100-fold more sonicate for equivalent nitrate production as wild-type BMDMs

hematopoietic system

abnormal macrophage physiology ( J:85323 )

• in vitro, mutant BMDMs do not respond to 500 ng/ml of B. burgdorferi recombinant OspA, as shown by a failure to elicit IL-6, IL-10, TNF and nitrate production relative to BMDMs from control C3H/HeN and C57BL/6 mice

• mutant BMDMs fail to respond to 5 um/ml OspA (a 10-fold higher concentration), as shown by a severely diminished production of nitrate, IL-6, IL-10, and TNF relative to wild-type BMDMs

• mutant BMDMs do respond to nonlipoprotein components of sonicated B. burgdorferi (N40) spirochetes, but require 10- to 100-fold more sonicate for equivalent nitrate production as wild-type BMDMs

• however, mutant BMDMs do show a strong response to repurified LPS (100 ng/ml)

decreased macrophage cytokine production ( J:85323 )

• TNF secretion by mutant BMDMs is abolished in response to 500 ng/ml of B. burgdorferi OspA

• TNF secretion by mutant BMDMs is severely reduced in response to 5 ug/ml of B. burgdorferi OspA

decreased macrophage nitric oxide production ( J:85323 )

• NO production by mutant BMDMs is abolished in response to 500 ng/ml of B. burgdorferi OspA

• NO production by mutant BMDMs is severely reduced in response to 5 ug/ml of B. burgdorferi OspA

• mutant BMDMs do respond to nonlipoprotein components of sonicated B. burgdorferi (N40) spirochetes, but require 10- to 100-fold more sonicate for equivalent nitrate production as wild-type BMDMs

Genotype
MGI:4452598

hm4

• Allelic Composition: Tlr2^tm1Kir/Tlr2^tm1Kir
• Genetic Background: involves: 129

mortality/aging

increased susceptibility to bacterial infection induced morbidity/mortality ( J:147177 )

• when infected with Sanger 476, a methicillin-susceptible S. aureus strain, or MW2, a methicillin-resistant S. aureus strain

immune system

abnormal interleukin secretion ( J:94463 )

decreased interleukin-1 secretion ( J:94463 )

• significantly reduced response to LPS challenge

decreased interleukin-6 secretion ( J:94463 )

• significantly reduced response to LPS challenge

decreased tumor necrosis factor secretion ( J:94463 )

• significantly reduced response to LPS challenge

increased susceptibility to bacterial infection induced morbidity/mortality ( J:147177 )

• when infected with Sanger 476, a methicillin-susceptible S. aureus strain, or MW2, a methicillin-resistant S. aureus strain

endocrine/exocrine glands

abnormal adrenal gland morphology ( J:94463 )

abnormal adrenal cortex morphology ( J:94463 )

• adrenal gland enlargement primarily involves the cortex

enlarged adrenal glands ( J:94463 )

abnormal adrenal gland secretion ( J:94463 )

• corticosterone production moderately decreased

homeostasis/metabolism

abnormal circulating corticosterone level ( J:94463 )

• lipopolysaccharide stimulation results in a smaller increase in plasma glucocorticoid than in controls

decreased circulating corticosterone level ( J:94463 )

• levels are significantly lower than in controls

• reduced further after lipoteichoic acid stimulation

abnormal circulating pituitary hormone level ( J:94463 )

• lipopolysaccharide stimulation results in very little increase in ACTH

increased circulating adrenocorticotropin level ( J:94463 )

• plasma ACTH is elevated

cellular

abnormal endoplasmic reticulum morphology ( J:94463 )

• little increase in smooth endoplasmic reticulum or liposome reduction in response to either lipopolysaccharide or lipoteichoic acid stimulation

abnormal mitochondrial morphology ( J:94463 )

abnormal mitochondrial shape ( J:94463 )

• increased folding of the mitochondrial membrane

decreased mitochondrial number ( J:94463 )

• in adrenocortical cells

Genotype
MGI:5428445

hm5

• Allelic Composition: Tlr2^tm1Kir/Tlr2^tm1Kir
• Genetic Background: involves: 129 * C57BL/6

nervous system

abnormal myelination ( J:161285 )

• hyaluronan is unable to block remyelination in the brain of lysolecithin treated homozygotes as it can in controls

Genotype
MGI:3574656

hm6

• Allelic Composition: Tlr2^tm1Kir/Tlr2^tm1Kir
• Genetic Background: Not Specified

mortality/aging

increased susceptibility to induced morbidity/mortality ( J:96018 )

• homozygous null mice succumbed to S. aureus infection within 5 days

immune system

abnormal macrophage physiology ( J:96018 )

• peritoneal macrophages were completely unresponsive and produced little or no TNF when stimulated with lipoteichoic acid (LTA) or macrophage-activating lipopeptide 2 (MALP-2) from Mycoplasma pneumoniae

increased susceptibility to bacterial infection ( J:96018 )

• during a 7-dap period, homozygous null mice were permissive for the growth of intradermally inoculated S. aureus, whereas the bacteria were cleared from wildtype

hematopoietic system

abnormal macrophage physiology ( J:96018 )

• peritoneal macrophages were completely unresponsive and produced little or no TNF when stimulated with lipoteichoic acid (LTA) or macrophage-activating lipopeptide 2 (MALP-2) from Mycoplasma pneumoniae

Genotype
MGI:5428446

cx7

• Allelic Composition: Ldlr^tm1Her/Ldlr^tm1Her; Tlr2^tm1Kir/Tlr2^tm1Kir
• Genetic Background: B6.129-Tlr2^tm1Kir Ldlr^tm1Her

homeostasis/metabolism

decreased circulating cholesterol level ( J:102502 )

• reduced total plasma cholesterol on a high fat diet relative to Ldlr^{tm1Her/tm1Her} controls

growth/size/body

increased body weight ( J:102502 , J:131783 )

• increased body weight on a high fat diet relative to Ldlr^{tm1Her/tm1Her} controls (J:102502)

cardiovascular system

atherosclerotic lesions ( J:102502 , J:131783 )

• aortic lesion area and aortic valve lesion volume are significantly reduced relative to Ldlr^{tm1Her/tm1Her} controls (J:102502)

• less lipid accumulation in the lesser aortic curvature on a high fat diet than in Ldlr^{tm1Her/tm1Her} controls (J:131783)

immune system

abnormal cellular extravasation ( J:131783 )

• leukocyte accumulation under the aortic endothelium is less than in Ldlr^{tm1Her/tm1Her} controls

decreased tumor necrosis factor secretion ( J:131783 )

• significantly reduced response to LPS challenge

cellular

abnormal cellular extravasation ( J:131783 )

• leukocyte accumulation under the aortic endothelium is less than in Ldlr^{tm1Her/tm1Her} controls

hematopoietic system

abnormal cellular extravasation ( J:131783 )

• leukocyte accumulation under the aortic endothelium is less than in Ldlr^{tm1Her/tm1Her} controls

Genotype
MGI:3706993

cx8

• Allelic Composition: Tlr2^tm1Kir/Tlr2^tm1Kir; Tlr4^tm1Aki/Tlr4^tm1Aki
• Genetic Background: B6.129-Tlr2^tm1Kir Tlr4^tm1Aki

mortality/aging

decreased susceptibility to induced morbidity/mortality ( J:121930 )

• systemic challenge with Myr3-CSK4 after D-galactosamine induces lethal shock in wild-type mice, but mutants are protected

• mice are resistant to lethal toxemia induced by heat-inactivated E. coli, whereas wild-type mice die

Genotype
MGI:3706988

cx9

• Allelic Composition: Tlr2^tm1Kir/Tlr2^tm1Kir; Tlr4^Lps-d/Tlr4^Lps-d
• Genetic Background: C3.Cg-Tlr2^tm1Kir Tlr4^Lps-d

mortality/aging

decreased susceptibility to induced morbidity/mortality ( J:121930 )

• after sensitization with D-galactosamine, 150 ug of Salmonella LPS does not cause lethal toxemia in double mutants, while all Tlr2-deficient single mutants die

• double mutants are protected from bacterial lipoteichoic acid exposure after priming by IFNgamma and sensitization with D-galactosamine, while Tlr4-deficient mice and wild-type are susceptible to lethal shock by this treatment

• systemic challenge with Myr₃-CSK₄ (a synthetic lipopeptide) after D-galactosamine induces lethal shock in wild-type mice, but mutants are protected

immune system

abnormal macrophage physiology ( J:121930 )

• high dose stimulation of macrophages by Pam₃-CSK₄ does not induce activation of the macrophages in contrast to activation of Tlr2-deficient macrophages

• priming with IFNgamma does not allow activation of macrophages upon stimulation by Pam₃-CSK₄

hematopoietic system

abnormal macrophage physiology ( J:121930 )

• high dose stimulation of macrophages by Pam₃-CSK₄ does not induce activation of the macrophages in contrast to activation of Tlr2-deficient macrophages

• priming with IFNgamma does not allow activation of macrophages upon stimulation by Pam₃-CSK₄

Genotype
MGI:7764767

cx10

• Allelic Composition: Tlr2^tm1Kir/Tlr2^tm1Kir; Tlr4^Lps-d/Tlr4^Lps-d
• Genetic Background: C.Cg-Tlr2^tm1Kir Tlr4^Lps-d

neoplasm

neoplasm ( J:329456 )

N • specific-pathogen free (SPF) offspring from mice infected with Rauscher-like murine leukemia virus (MuLV infected offspring) exhibit leukemia latency and incidence similar to wild-type specific-pathogen free mice

Genotype
MGI:5428447

cx11

• Allelic Composition: Tlr2^tm1Kir/Tlr2^tm1Kir; Tg(APP695)3Dbo/?; Tg(PSEN1)5Dbo/?
• Genetic Background: involves: 129 * C3H/HeJ * C57BL/6

behavior/neurological

impaired passive avoidance behavior ( J:136387 )

• retention is reduced in passive avoidance tests involving electric shock training to prevent movement from a lighted area to a dark chamber

abnormal long-term spatial reference memory ( J:136387 )

• retention of spatial memory in T-water maze tests declines as early as 3 months after acquisition, faster than for transgenics alone

• acquisition of spatial memory in T-water maze tests is normal

nervous system

amyloid beta deposits ( J:136387 )

• lower rate of plaque deposition at 3 and 6 months of age but equivalent to controls at 9 months

• higher brain levels of Abeta1-42

homeostasis/metabolism

amyloid beta deposits ( J:136387 )

• lower rate of plaque deposition at 3 and 6 months of age but equivalent to controls at 9 months

• higher brain levels of Abeta1-42