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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Trem2tm1(KOMP)Vlcg
targeted mutation 1, Velocigene
MGI:3797897
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Trem2tm1(KOMP)Vlcg/Trem2tm1(KOMP)Vlcg C57BL/6N-Trem2tm1(KOMP)Vlcg MGI:5897237
cx2
Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr/0
Trem2tm1(KOMP)Vlcg/Trem2+
involves: C57BL/6J * C57BL/6NTac MGI:6198555


Genotype
MGI:5897237
hm1
Allelic
Composition
Trem2tm1(KOMP)Vlcg/Trem2tm1(KOMP)Vlcg
Genetic
Background
C57BL/6N-Trem2tm1(KOMP)Vlcg
Cell Lines 10093A-A4
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trem2tm1(KOMP)Vlcg mutation (1 available); any Trem2 mutation (68 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• in culture, primary microglia isolated from newborn pups exhibit an increased number of TUNEL+ apoptotic cells relative to wild-type microglia
• protein level of cleaved Caspase-3 (c-Casp3) is increased in microglia cell lysates, whereas protein levels of pro-Caspase3 (the inactive precursor to c-Casp3) and Bcl-2 (an anti-apoptotic protein) are decreased, suggesting accelerated microglial apoptosis
• decreased cell viability (survival) in microglia, as assessed by MTT assay
• decreased microglia cell proliferation, as shown by BrdU incorporation assay
• in culture, primary microglia isolated from newborn pups exhibit an increased number of TUNEL+ apoptotic cells relative to wild-type microglia
• microglia show accelerated degradation of beta-catenin and severe downregulation of Wnt/beta-catenin signaling; beta-catenin levels, microglial cell survival and proliferation can be partially restored by Wnt3a or LiCl or TDZD-8 treatment
• following neuronal injury induced by kainic acid treatment, mice exhibit decreased microgliosis with significantly reduced morphological changes and number of activated microglia relative to wild-type controls, esp. in the hippocampus

cellular
• FACS analysis of microglia revealed an accumulation of cells in the G0/G1 phase of the cell cycle and a decreased percentage of cells in the S phase, indicating cell cycle arrest at the G1/S checkpoint
• mRNA and protein levels of Cyclin D1 and c-Myc are significantly decreased relative to those in wild-type microglia
• in culture, primary microglia isolated from newborn pups exhibit an increased number of TUNEL+ apoptotic cells relative to wild-type microglia
• protein level of cleaved Caspase-3 (c-Casp3) is increased in microglia cell lysates, whereas protein levels of pro-Caspase3 (the inactive precursor to c-Casp3) and Bcl-2 (an anti-apoptotic protein) are decreased, suggesting accelerated microglial apoptosis

immune system
• decreased cell viability (survival) in microglia, as assessed by MTT assay
• decreased microglia cell proliferation, as shown by BrdU incorporation assay
• in culture, primary microglia isolated from newborn pups exhibit an increased number of TUNEL+ apoptotic cells relative to wild-type microglia
• microglia show accelerated degradation of beta-catenin and severe downregulation of Wnt/beta-catenin signaling; beta-catenin levels, microglial cell survival and proliferation can be partially restored by Wnt3a or LiCl or TDZD-8 treatment
• following neuronal injury induced by kainic acid treatment, mice exhibit decreased microgliosis with significantly reduced morphological changes and number of activated microglia relative to wild-type controls, esp. in the hippocampus

hematopoietic system
• decreased cell viability (survival) in microglia, as assessed by MTT assay
• decreased microglia cell proliferation, as shown by BrdU incorporation assay
• in culture, primary microglia isolated from newborn pups exhibit an increased number of TUNEL+ apoptotic cells relative to wild-type microglia
• microglia show accelerated degradation of beta-catenin and severe downregulation of Wnt/beta-catenin signaling; beta-catenin levels, microglial cell survival and proliferation can be partially restored by Wnt3a or LiCl or TDZD-8 treatment
• following neuronal injury induced by kainic acid treatment, mice exhibit decreased microgliosis with significantly reduced morphological changes and number of activated microglia relative to wild-type controls, esp. in the hippocampus




Genotype
MGI:6198555
cx2
Allelic
Composition
Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr/0
Trem2tm1(KOMP)Vlcg/Trem2+
Genetic
Background
involves: C57BL/6J * C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr mutation (1 available)
Trem2tm1(KOMP)Vlcg mutation (1 available); any Trem2 mutation (68 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• mice show a reduction in the number of plaque-associated myeloid cells compared to single transgenic Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr mice, indicating an impairment in myeloid cell accumulation around plaques
• proliferation of myeloid cells is reduced compared to levels in single transgenic Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr mice

homeostasis/metabolism
• mice exhibit a modest increase in the total cortical plaque number and percent area compared to single transgenic Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr mice
• mice show an increase in soluble amyloid beta 1-40 in the hippocampus compared to single transgenic Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr mice

nervous system
• mice exhibit a modest increase in the total cortical plaque number and percent area compared to single transgenic Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr mice
• mice show an increase in soluble amyloid beta 1-40 in the hippocampus compared to single transgenic Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr mice
• marker analysis indicates increased plaque-associated neuritic dystrophy compared to single transgenic Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr mice





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last database update
11/12/2024
MGI 6.24
The Jackson Laboratory