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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Mertktm1Gkm
targeted mutation 1, Glenn K Matsushima
MGI:2387768
Summary 6 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Mertktm1Gkm/Mertktm1Gkm B6.129P2-Mertktm1Gkm MGI:3844821
hm2
Mertktm1Gkm/Mertktm1Gkm involves: 129P2/OlaHsd MGI:3844732
hm3
Mertktm1Gkm/Mertktm1Gkm involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:3844702
hm4
Mertktm1Gkm/Mertktm1Gkm NOD.129P2-Mertktm1Gkm MGI:3844819
ht5
Mertknmf12/Mertktm1Gkm involves: 129P2/OlaHsd * C57BL/6J MGI:5287879
cx6
Mertktm1Gkm/Mertktm1Gkm
Tg(TcraBDC2.5,TcrbBDC2.5)1Doi/0
NOD.Cg-Mertktm1Gkm Tg(TcraBDC2.5,TcrbBDC2.5)1Doi MGI:3844820


Genotype
MGI:3844821
hm1
Allelic
Composition
Mertktm1Gkm/Mertktm1Gkm
Genetic
Background
B6.129P2-Mertktm1Gkm
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mertktm1Gkm mutation (0 available); any Mertk mutation (63 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• mice injected with spleen cells from H2-Ab1 homozygotes fail to exhibit an increase in autoantibodies unlike in wild-type mice
• when B cells are used in adoptive transfer into Rag knock-out mice that were then challenged with spleen cells from H2-Ab1 homozygotes mice fail to develop autoantibodies
• mice injected with spleen cells from H2-Ab1 homozygotes fail to exhibit an increase in autoantibodies, splenomegaly, and mild ascites unlike in wild-type mice
• however, splenocytes from H2-Ab1 homozygotes proliferate normally in response to spleen cells, allogenic stimulus has some effect on B cells, and B cells have autoreactive potential




Genotype
MGI:3844732
hm2
Allelic
Composition
Mertktm1Gkm/Mertktm1Gkm
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mertktm1Gkm mutation (0 available); any Mertk mutation (63 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
vision/eye
• at 6 months, strands of nuclei from the inner nuclear layer begin to cross the inner plexiform layer towards the ganglion cell layer
• at 6 months of age, retinal capillaries invade the retinal pigment epithelium unlike in wild-type mice
• at 8 months, retinal pigment epithelium invades the retina and localizes along retinal blood vessels unlike in wild-type mice
• at P20, the rod outer segment is longer than in wild-type mice and results in a 67% greater concentration of rhodopsin than in wild-type mice
• by P60, all outer segment membranes and rhodopsin are undetectable unlike in wild-type mice
• unlike in wild-type retinas, vacuoles containing delicate fragments of outer segment membranes are observed
• at later ages, a debris zone from the degenerating outer segment replaces the inner segment and outer segment layer
• however, by P45 the debris zone has largely disappeared
• beyond P45, mice exhibit retinal rod cell degeneration unlike in wild-type mice
• however, no hemispheric difference in the degeneration is observed
• early in degeneration, membranous whorls are present on the retinal pigment epithelium unlike in wild-type mice
• however, by P45 the whorls have largely disappeared
• few, if any, phagosome are found in the retinal pigment epithelium at the peak period of rod outer disc shedding unlike in wild-type mice
• at 6 months of age, retinal capillaries invade the retinal pigment epithelium unlike in wild-type mice
• at 8 months, retinal pigment epithelium invades the retina and localizes along retinal blood vessels unlike in wild-type
• at P45, small focal thinning in the retinal pigment epithelium is observed unlike in wild-type mice
• however, some retinal pigment epithelium is thicker than normal
• at P40, 70% of cells in the outer nuclear layer are pyknotic unlike in wild-type mice
• at P20, invading macrophages or microglia are observed in the outer nuclear layer unlike in wild-type mice
• progressive thinning of the retinal outer nuclear layer (ONL) beginning at P25 with less than one row of cell nuclei remaining by P45
• at a similar, if not slightly more rapid, rate of degeneration in pink-eyed RCS rats
• at P33, photopic amplitudes are lower than normal
• at P33, photopic implicit time is delayed 75% compared to in wild-type mice
• photopic b wave amplitudes and implicit times decline rapidly with age
• no clear a or b waves are detected beyond P40 in some mice
• at P30, scotopic a and b waves are lower than normal
• at P33, scotopic implicit time is delayed 75% compared to in wild-type mice
• scotopic a and b wave amplitudes and implicit times decline rapidly with age
• no clear a or b waves are detected beyond P40 in some mice
• at P33 and older, scotopic threshold response is higher than in wild-type mice
• however, scotopic threshold response is measurable at bright stimulus intensities when only scattered PR nuclei remain as late as P253

cardiovascular system
• at 6 months of age, retinal capillaries invade the retinal pigment epithelium unlike in wild-type mice
• at 8 months, retinal pigment epithelium invades the retina and localizes along retinal blood vessels unlike in wild-type mice

nervous system
• at P20, the rod outer segment is longer than in wild-type mice and results in a 67% greater concentration of rhodopsin than in wild-type mice
• by P60, all outer segment membranes and rhodopsin are undetectable unlike in wild-type mice
• unlike in wild-type retinas, vacuoles containing delicate fragments of outer segment membranes are observed
• at later ages, a debris zone from the degenerating outer segment replaces the inner segment and outer segment layer
• however, by P45 the debris zone has largely disappeared
• beyond P45, mice exhibit retinal rod cell degeneration unlike in wild-type mice
• however, no hemispheric difference in the degeneration is observed

pigmentation
• early in degeneration, membranous whorls are present on the retinal pigment epithelium unlike in wild-type mice
• however, by P45 the whorls have largely disappeared
• few, if any, phagosome are found in the retinal pigment epithelium at the peak period of rod outer disc shedding unlike in wild-type mice
• at 6 months of age, retinal capillaries invade the retinal pigment epithelium unlike in wild-type mice
• at 8 months, retinal pigment epithelium invades the retina and localizes along retinal blood vessels unlike in wild-type
• at P45, small focal thinning in the retinal pigment epithelium is observed unlike in wild-type mice
• however, some retinal pigment epithelium is thicker than normal




Genotype
MGI:3844702
hm3
Allelic
Composition
Mertktm1Gkm/Mertktm1Gkm
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mertktm1Gkm mutation (0 available); any Mertk mutation (63 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• the 100% lethal dose (LD100) of LPS-treated mice exhibit is half the concentration as the LD100 of similarly treated wild-type mice
• however, pre-treatment of mice with anti-TNF-alpha antibodies prior to LPS treatment protects them from lethal sepsis

immune system
• serum TNF-alpha levels in LPS treated mice are 3-fold higher than in similarly treated wild-type mice
• LPS-treated macrophages secrete more TNF-alpha than similarly treated wild-type cells
• LPS-treated macrophages secrete more TNF-alpha than similarly treated wild-type cells
• the 100% lethal dose (LD100) of LPS-treated mice exhibit is half the concentration as the LD100 of similarly treated wild-type mice
• LPS-treated mice exhibit increased lesions and hemorrhagic necrosis in the bowel with greater fluid accumulation, an increase infiltration of red blood cells and leukocytes into the villi, and degeneration of villi compared to in similarly-treated wild-type mice
• serum TNF-alpha levels in LPS treated mice are 3-fold higher than in similarly treated wild-type mice
• however, pre-treatment of mice with anti-TNF-alpha antibodies prior to LPS treatment protects them from lethal sepsis

digestive/alimentary system
• LPS-treated mice exhibit increased lesions and hemorrhagic necrosis in the bowel with greater fluid accumulation, an increase infiltration of red blood cells and leukocytes into the villi, and degeneration of villi compared to in similarly-treated wild-type mice

homeostasis/metabolism
• serum TNF-alpha levels in LPS treated mice are 3-fold higher than in similarly treated wild-type mice




Genotype
MGI:3844819
hm4
Allelic
Composition
Mertktm1Gkm/Mertktm1Gkm
Genetic
Background
NOD.129P2-Mertktm1Gkm
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mertktm1Gkm mutation (0 available); any Mertk mutation (63 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Mononuclear cell infiltration of the large intestines and salivary glands are reduced in Mertktm1Gkm/Mertktm1Gkm mice

immune system
• thymic dendritic cells pulsed with BDC induce more apoptosis in cocultured NOD thymocytes expressing Tg(TcraBDC2.5)1Doi Tg(TcrbBDC2.5)2Doi compared to heterozygous cells without altering phenotypic markers for dendritic cell activation and maturation
• few mice develop insulitis by 12 and 17 weeks of age
• infiltrate into islet cells is composed of mostly B cells and CD8+ T cells with few CD4+ T cells unlike in heterozygous mice
• beta cell-specific T cells are reduced in the islet cells compared to in heterozygous mice
• at 12 weeks of age, the frequency of islet-infiltrating CD4+ and CD8+ T cells secreting IFN-gamma is reduced compared to in heterozygotes
• at 12 weeks, the frequency of NRP-V7-specific CD8+ T cells in islet infiltrate is decreased compared to in heterozygous mice
• mice exhibit reduced mononuclear cell infiltrate in the large intestines and salivary glands compared to in NOD mice
• beta cell-specific T cells are reduced in the islet cells compared to in heterozygous mice
• female mice do not develop diabetes by 52 weeks of age unlike heterozygous mice
• when bone marrow cells are used to reconstitute irradiated NOD mice recipients remain diabetes free
• however, irradiated mice reconstituted with NOD bone marrow develop diabetes

endocrine/exocrine glands
• few mice develop insulitis by 12 and 17 weeks of age
• infiltrate into islet cells is composed of mostly B cells and CD8+ T cells with few CD4+ T cells unlike in heterozygous mice
• beta cell-specific T cells are reduced in the islet cells compared to in heterozygous mice
• at 12 weeks of age, the frequency of islet-infiltrating CD4+ and CD8+ T cells secreting IFN-gamma is reduced compared to in heterozygotes
• at 12 weeks, the frequency of NRP-V7-specific CD8+ T cells in islet infiltrate is decreased compared to in heterozygous mice

hematopoietic system
• thymic dendritic cells pulsed with BDC induce more apoptosis in cocultured NOD thymocytes expressing Tg(TcraBDC2.5)1Doi Tg(TcrbBDC2.5)2Doi compared to heterozygous cells without altering phenotypic markers for dendritic cell activation and maturation
• mice exhibit reduced mononuclear cell infiltrate in the large intestines and salivary glands compared to in NOD mice
• beta cell-specific T cells are reduced in the islet cells compared to in heterozygous mice

cellular
• thymic dendritic cells pulsed with BDC induce more apoptosis in cocultured NOD thymocytes expressing Tg(TcraBDC2.5)1Doi Tg(TcrbBDC2.5)2Doi compared to heterozygous cells without altering phenotypic markers for dendritic cell activation and maturation




Genotype
MGI:5287879
ht5
Allelic
Composition
Mertknmf12/Mertktm1Gkm
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mertknmf12 mutation (1 available); any Mertk mutation (63 available)
Mertktm1Gkm mutation (0 available); any Mertk mutation (63 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
vision/eye
• pan-retinal fundus patches
• severe photoreceptor loss in the peripheral retina

nervous system
• severe photoreceptor loss in the peripheral retina




Genotype
MGI:3844820
cx6
Allelic
Composition
Mertktm1Gkm/Mertktm1Gkm
Tg(TcraBDC2.5,TcrbBDC2.5)1Doi/0
Genetic
Background
NOD.Cg-Mertktm1Gkm Tg(TcraBDC2.5,TcrbBDC2.5)1Doi
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mertktm1Gkm mutation (0 available); any Mertk mutation (63 available)
Tg(TcraBDC2.5,TcrbBDC2.5)1Doi mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• the frequency of double positive T cell apoptosis in thymic lobes is increased compared to in similarly treated heterozygous mice
• fetal thymic organ cultures treated with BDC2.5 produce fewer double positive thymocytes than similarly treated heterozygous cells
• fetal thymic organ cultures treated with BDC2.5 produce more CD8+ single positive thymocytes than similarly treated heterozygous cells

hematopoietic system
• the frequency of double positive T cell apoptosis in thymic lobes is increased compared to in similarly treated heterozygous mice
• fetal thymic organ cultures treated with BDC2.5 produce fewer double positive thymocytes than similarly treated heterozygous cells
• fetal thymic organ cultures treated with BDC2.5 produce more CD8+ single positive thymocytes than similarly treated heterozygous cells

cellular
• the frequency of double positive T cell apoptosis in thymic lobes is increased compared to in similarly treated heterozygous mice





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last database update
04/16/2024
MGI 6.23
The Jackson Laboratory