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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Atg7tm1Tchi
targeted mutation 1, Tomoki Chiba
MGI:3587769
Summary 26 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Atg7tm1Tchi/Atg7tm1Tchi
Sqstm1tm1Keta/Sqstm1tm1Keta
Tg(Mx1-cre)1Cgn/0
involves: 129 * C57BL/6 * C57BL/6NCrlj * CBA * CBA/JNCrlj MGI:3806622
cn2
Atg7tm1Tchi/Atg7tm1Tchi
Sqstm1tm1Keta/Sqstm1tm1Keta
Tg(Nes-cre)1Wme/0
involves: 129 * C57BL/6 * C57BL/6NCrlj * CBA * CBA/JNCrlj MGI:3806624
cn3
Alpltm1(cre)Nagy/Alpl+
Atg7tm1Tchi/Atg7tm1Tchi
involves: 129 * C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj MGI:6870513
cn4
Atg7tm1Tchi/Atg7tm1Tchi
Lyz2tm1(cre)Ifo/Lyz2+
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * DBA/2 MGI:6287974
cn5
Apctm2.1Cip/Apc+
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Vil1-cre/ERT2)23Syr/0
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * DBA/2 MGI:5702420
cn6
Atg7tm1Tchi/Atg7tm1Tchi
Aviltm2(cre)Fawa/Avil+
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:4460014
cn7
Atg7tm1Tchi/Atg7tm1Tchi
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6NCrlj * CBA/JNCrlj MGI:6287973
cn8
Atg7tm1Tchi/Atg7tm1Tchi
Cnot3tm1.1Kjkb/Cnot3tm1.1Kjkb
Tg(Ckmm-cre)5Khn/0
involves: 129P2/OlaHsd * C57BL/6NCrlj * CBA/JNCrlj * FVB MGI:6151152
cn9
Atg7tm1Tchi/Atg7tm1Tchi
Cnot3tm1.1Kjkb/Cnot3tm1.1Kjkb
A1cfTg(Myh6-cre/Esr1*)1Jmk/A1cf+
involves: 129P2/OlaHsd * C57BL/6NCrlj * CBA/JNCrlj * FVB/N MGI:6151155
cn10
Atg7tm1Tchi/Atg7tm1Tchi
Cnot3tm1.1Kjkb/Cnot3tm1.1Kjkb
A1cfTg(Myh6-cre/Esr1*)1Jmk/A1cfTg(Myh6-cre/Esr1*)1Jmk
involves: 129P2/OlaHsd * C57BL/6NCrlj * CBA/JNCrlj * FVB/N MGI:6151156
cn11
Atg7tm1Tchi/Atg7tm1Tchi
En1tm2(cre)Wrst/En1+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6NCrlj * CBA/JNCrlj MGI:5471363
cn12
Atg7tm1Tchi/Atg7tm1Tchi
Slc6a3tm1(cre)Xz/Slc6a3+
involves: 129S1/Sv * C57BL/6NCrlj * CBA/JNCrlj MGI:5471365
cn13
Tsc2tm1Djk/Tsc2+
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Camk2a-cre)T29-1Stl/0
involves: 129S4/SvJae * BALB/c * C57BL * C57BL/6 * CBA/JNCrlj MGI:5824126
cn14
Atg7tm1Tchi/Atg7tm1Tchi
Xbp1tm2Glm/Xbp1tm2Glm
Tg(Defa6-icre)1Rsb/0
involves: 129S6/SvEvTac * C57BL/6 * CBA MGI:5559516
cn15
Atg7tm1Tchi/Atg7tm1Tchi
Xbp1tm2Glm/Xbp1tm2Glm
Tg(Vil1-cre)997Gum/0
involves: 129S6/SvEvTac * C57BL/6 * CBA * SJL MGI:5559519
cn16
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Camk2a-cre)T29-1Stl/0
involves: BALB/c * C57BL * C57BL/6J * C57BL/6NCrlj * CBA/JNCrlj MGI:5824124
cn17
Atg7tm1Tchi/Atg7tm1Tchi
Tg(SLC18A3-cre)KMisa/0
involves: C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj MGI:5470096
cn18
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Tyr-cre)1Lru/Y
involves: C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * DBA/2 MGI:6209426
cn19
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Nes-cre)1Kln/0
Wdr45btm1c(EUCOMM)Hmgu/Wdr45btm1c(EUCOMM)Hmgu
involves: C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * SJL MGI:6480015
cn20
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Mx1-cre)1Cgn/0
involves: C57BL/6 * CBA MGI:3590137
cn21
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Nes-cre)1Wme/0
involves: C57BL/6 * CBA MGI:3806620
cn22
Atg7tm1Tchi/Atg7tm1Tchi
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6J * C57BL/6NCrlj * CBA/JNCrlj MGI:6870515
cn23
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Vil1-cre)1000Gum/0
involves: C57BL/6J * C57BL/6NCrlj * CBA/JNCrlj * SJL/J MGI:5569387
cn24
Atg7tm1Tchi/Atg7tm1Tchi
Commd10Tg(Vav1-icre)A2Kio/Commd10+
involves: C57BL/6NCrlj * C57BL/10 * CBA/Ca * CBA/JNCrlj MGI:5295638
cn25
Atg7tm1Tchi/Atg7tm1Tchi
Cnot1tm1Tya/Cnot1tm1Tya
Tg(Ckmm-cre)5Khn/0
involves: C57BL/6NCrlj * CBA/JNCrlj * FVB MGI:6151162
cn26
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Nes-cre)1Kln/0
involves: C57BL/6NCrlj * CBA/JNCrlj * SJL MGI:6480014


Genotype
MGI:3806622
cn1
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Sqstm1tm1Keta/Sqstm1tm1Keta
Tg(Mx1-cre)1Cgn/0
Genetic
Background
involves: 129 * C57BL/6 * C57BL/6NCrlj * CBA * CBA/JNCrlj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Sqstm1tm1Keta mutation (0 available); any Sqstm1 mutation (35 available)
Tg(Mx1-cre)1Cgn mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• slightly eleveated levels of ALT are found in the sera after Cre-induction but not to the degree of conditional knockouts with wild-type Sqstm1 alleles
• high levels of ALP are found in the sera after Cre-induction but not to the degree of conditional knockouts with wild-type Sqstm1 alleles
• slightly elevated levels of AST are found in the sera after Cre-induction but not to the degree of conditional knockouts with wild-type Sqstm1 alleles

liver/biliary system
• the cytoplasmic inclusion bodies containing ubiquitinated proteins that are associated with Atg7 conditional liver knockout mice are almost completely absent in these mice
• liver function is slightly decreased after Cre-induction but not to the degree of conditional knockouts with wild-type Sqstm1 alleles




Genotype
MGI:3806624
cn2
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Sqstm1tm1Keta/Sqstm1tm1Keta
Tg(Nes-cre)1Wme/0
Genetic
Background
involves: 129 * C57BL/6 * C57BL/6NCrlj * CBA * CBA/JNCrlj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Sqstm1tm1Keta mutation (0 available); any Sqstm1 mutation (35 available)
Tg(Nes-cre)1Wme mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• large pyramidal neurons in the hippocampus are absent
• large pyramidal neurons in the cerebral cortex are absent
• Purkinje cells in the cerebellum are absent in these mice
• myelinated axons of the cerebellar nuclei are frequently enlarged and contain aberrant membranous structures and degenerated materials
• the cytoplasmic inclusion bodies containing ubiquitinated proteins that are found in the brain of Atg7 conditional knockouts are largely absent in these mice
• increased apoptosis of the neurons occurs in the cerebellar nucleus and the cerebral cortex

behavior/neurological
• abnormal limb clasping is observed in mice
• is observed

cellular
• increased apoptosis of the neurons occurs in the cerebellar nucleus and the cerebral cortex




Genotype
MGI:6870513
cn3
Allelic
Composition
Alpltm1(cre)Nagy/Alpl+
Atg7tm1Tchi/Atg7tm1Tchi
Genetic
Background
involves: 129 * C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Alpltm1(cre)Nagy mutation (6 available); any Alpl mutation (352 available)
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• total number of spermatozoa in the cauda epididymis is severely reduced
• acrosomes fail to acquire the characteristic crescent moon shape and display various defects, including mislocalization, deformation and fragmentation
• fragmented acrosomes are observed in the Golgi and cap phases
• acrosome shrinkage is detected in the cap phase due to accumulated proacrosomal vesicles derived from the Golgi apparatus
• vacuolated or irregularly shaped acrosomes are seen in subsequent stages of spermiogenesis
• acrosome biogenesis is disrupted starting in the Golgi phase: multiple small vesicles are localized to the perinuclear region without fusing with each other in ~30% of Golgi-phase spermatids
• in the cap-phase, the acrosome fails to spread normally along the nucleus and many proacrosomal vesicles accumulate in the concave region near the trans-Golgi stacks in ~27% of spermatids
• in the acrosome and maturation phases, irregular or roughly round acrosomes are found in ~24% of spermatids and the nucleus shows less chromatin condensation and/or impaired nuclear elongation
• defect in acrosome formation is most likely due to the failure of Golgi-derived proacrosomal vesicle fusion and/or membrane trafficking
• multiple small vesicles are localized to the perinuclear region without fusing with each other in ~30% of Golgi-phase spermatids
• TEM images show two proacrosomal centers present around the nucleus
• 26.80% of sperm exhibit irregularly shaped round heads, only seen in 0.42% of control sperm
• in the acrosome and maturation phases, the nucleus neighboring malformed acrosomes shows less chromatin condensation and/or impaired nuclear elongation, resulting in round or irregularly shaped nuclei
• TUNEL staining showed a significantly higher % of apoptotic cells in the seminiferous tubules (0.47% versus 0.04% in control tubules)
• seminiferous tubule structure appears disorganized: 36.67% of tubules contain large vacuoles in their lumen versus only 1.33% of control tubules
• TUNEL staining showed a significantly higher % of apoptotic cells in the seminiferous tubules (0.47% versus 0.04% in control tubules)
• however, seminiferous tubule diameter is normal
• testis size is significantly smaller than that in control males
• testis weight is significantly lower than that in control males
• acrosome biogenesis is highly disrupted during early stages of spermiogenesis
• many detached premature germ cells and abnormal spermatozoa are detected in the cauda epididymis
• males are almost completely infertile: when mated to wild-type females for a 2-month period, pregnancy rate is only 8.14% versus 87.01% for control males
• in vivo fertilization capacity of spermatozoa is impaired; when male mice are mated with wild-type females, no 2-cell embryos are obtained
• however, this defect is successfully rescued by intracytoplasmic sperm injections
• in vitro, the rate of A23187-induced acrosome reaction is severely reduced: after induction, only 38.67% of spermatozoa show loss of their PSA-positive structures versus 63.87% in control sperm, suggesting failure to release acrosomal contents
• however, the rate of spontaneous acrosome reaction is relatively normal

cellular
• total number of spermatozoa in the cauda epididymis is severely reduced
• acrosomes fail to acquire the characteristic crescent moon shape and display various defects, including mislocalization, deformation and fragmentation
• fragmented acrosomes are observed in the Golgi and cap phases
• acrosome shrinkage is detected in the cap phase due to accumulated proacrosomal vesicles derived from the Golgi apparatus
• vacuolated or irregularly shaped acrosomes are seen in subsequent stages of spermiogenesis
• acrosome biogenesis is disrupted starting in the Golgi phase: multiple small vesicles are localized to the perinuclear region without fusing with each other in ~30% of Golgi-phase spermatids
• in the cap-phase, the acrosome fails to spread normally along the nucleus and many proacrosomal vesicles accumulate in the concave region near the trans-Golgi stacks in ~27% of spermatids
• in the acrosome and maturation phases, irregular or roughly round acrosomes are found in ~24% of spermatids and the nucleus shows less chromatin condensation and/or impaired nuclear elongation
• defect in acrosome formation is most likely due to the failure of Golgi-derived proacrosomal vesicle fusion and/or membrane trafficking
• multiple small vesicles are localized to the perinuclear region without fusing with each other in ~30% of Golgi-phase spermatids
• TEM images show two proacrosomal centers present around the nucleus
• 26.80% of sperm exhibit irregularly shaped round heads, only seen in 0.42% of control sperm
• in the acrosome and maturation phases, the nucleus neighboring malformed acrosomes shows less chromatin condensation and/or impaired nuclear elongation, resulting in round or irregularly shaped nuclei
• autophagic flux is disrupted in the testis, as indicated by a 1.5-fold increase in polyubiquitinated protein level and accumulation of the autophagic substrate SQSTM1/p62 and of LC3-I but not the membrane-associated form LC3-II
• TUNEL staining showed a significantly higher % of apoptotic cells in the seminiferous tubules (0.47% versus 0.04% in control tubules)

homeostasis/metabolism
• autophagic flux is disrupted in the testis, as indicated by a 1.5-fold increase in polyubiquitinated protein level and accumulation of the autophagic substrate SQSTM1/p62 and of LC3-I but not the membrane-associated form LC3-II

endocrine/exocrine glands
• seminiferous tubule structure appears disorganized: 36.67% of tubules contain large vacuoles in their lumen versus only 1.33% of control tubules
• TUNEL staining showed a significantly higher % of apoptotic cells in the seminiferous tubules (0.47% versus 0.04% in control tubules)
• however, seminiferous tubule diameter is normal
• testis size is significantly smaller than that in control males
• testis weight is significantly lower than that in control males




Genotype
MGI:6287974
cn4
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Lyz2tm1(cre)Ifo/Lyz2+
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Lyz2tm1(cre)Ifo mutation (14 available); any Lyz2 mutation (40 available)
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• mice injected with UV-irradiated dying thymocytes into the spleen, liver, or kidney exhibit defective clearance of engulfed, dying cells and no induction of LC3-II, indicating failure of LC3-associated phagocytosis-dependent mechanism to degrade engulfed corpses

homeostasis/metabolism
• serum CCL4 levels are increased in mice injected with UV-irradiated dying thymocytes
• serum IL-1beta levels are increased in mice injected with UV-irradiated dying thymocytes
• serum IL-10 levels are not increased in mutant mice injected with UV-irradiated dying thymocytes like in wild-type mice
• serum IL-6 levels are increased in mice injected with UV-irradiated dying thymocytes

immune system
• mice injected with UV-irradiated dying thymocytes into the spleen, liver, or kidney exhibit defective clearance of engulfed, dying cells and no induction of LC3-II, indicating failure of LC3-associated phagocytosis-dependent mechanism to degrade engulfed corpses
• serum CCL4 levels are increased in mice injected with UV-irradiated dying thymocytes
• serum IL-1beta levels are increased in mice injected with UV-irradiated dying thymocytes
• serum IL-10 levels are not increased in mutant mice injected with UV-irradiated dying thymocytes like in wild-type mice
• serum IL-6 levels are increased in mice injected with UV-irradiated dying thymocytes




Genotype
MGI:5702420
cn5
Allelic
Composition
Apctm2.1Cip/Apc+
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Vil1-cre/ERT2)23Syr/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm2.1Cip mutation (2 available); any Apc mutation (158 available)
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Tg(Vil1-cre/ERT2)23Syr mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• tamoxifen treated mice show fewer and smaller colonic tumors that develop more slowly and have a lower proliferation rate than in single conditional Apc heterozygous mice
• however, prolonged antibiotic treatment of tamoxifen treated mice induces numerous intestinal tumor foci and tamoxifen treated mice administered anti-CD8 antibodies to induce partial depletion of Treg show increased tumor development

digestive/alimentary system
• abnormal accumulation of granules of mucus in goblet cells in the tumor-free mucosa of tamoxifen treated mice
• unusually small in tumor-free mucosa of tamoxifen treated mice
• tamoxifen treated mice show fewer and smaller colonic tumors that develop more slowly and have a lower proliferation rate than in single conditional Apc heterozygous mice
• however, prolonged antibiotic treatment of tamoxifen treated mice induces numerous intestinal tumor foci and tamoxifen treated mice administered anti-CD8 antibodies to induce partial depletion of Treg show increased tumor development
• tamoxifen treated mice show altered distribution of gut bacteria, with bacteria occasionally seen within the crypt compartment of the small intestine
• tamoxifen treated mice show a difference in the overall composition of both fecal and ileal microbiota compared to single conditional Apc heterozygotes, with mice showing a high level of Gram+ bacteria related to Firmicutes and low levels of Proteobacteria in feces
• ileal mucosa of tamoxifen treated mice has a higher bacterial diversity than single conditional Apc heterozygotes
• intestinal permeability is high in tamoxifen treated mice

endocrine/exocrine glands
• unusually small in tumor-free mucosa of tamoxifen treated mice

hematopoietic system
• proportion of CD103+CD11b- dendritic cell subset involved in T-cell priming is higher in tamoxifen treated mice than in single conditional Apc heterozygous mice
• the number of Treg and CD8 IFN-gamma T cells in the lamina propria is higher than in single conditional Apc heterozygous mice
• administration of IL-1beta receptor antagonist, anakinra, to tamoxifen treated mice is sufficient to prevent the expansion of cytotoxic CD8+ T cells
• the number of Treg and CD8 IFN-gamma T cells in the lamina propria is higher than in single conditional Apc heterozygous mice

immune system
• proportion of CD103+CD11b- dendritic cell subset involved in T-cell priming is higher in tamoxifen treated mice than in single conditional Apc heterozygous mice
• the number of Treg and CD8 IFN-gamma T cells in the lamina propria is higher than in single conditional Apc heterozygous mice
• administration of IL-1beta receptor antagonist, anakinra, to tamoxifen treated mice is sufficient to prevent the expansion of cytotoxic CD8+ T cells
• the number of Treg and CD8 IFN-gamma T cells in the lamina propria is higher than in single conditional Apc heterozygous mice
• tamoxifen treated mice show marked infiltration of lymphocytes within the normal mucosa, higher numbers of CD45 and T cells in the small intestine and colon mucosa, influx of CD11c+ cells in the intestinal mucosa compared to single conditional Apc heterozygous mice, indicating promotion of anti-tumor immune responses
• immune cells isolated from the lamina propria of tamoxifen treated mice produce high amounts of IL-1beta
• immune cells isolated from the lamina propria of tamoxifen treated mice produce high amounts of IL-10

cellular
• abnormal accumulation of granules of mucus in goblet cells in the tumor-free mucosa of tamoxifen treated mice




Genotype
MGI:4460014
cn6
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Aviltm2(cre)Fawa/Avil+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Aviltm2(cre)Fawa mutation (2 available); any Avil mutation (47 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• at 9 months in the dorsal root ganglia
• at 9 months
• at 9 months, neurons contain large inclusion bodies and numerous electron-dense organelles unlike in wild-type mice
• at 9 months, mice exhibit neurodegeneration of TrkA+, cRet+, TrkB+, and TrkC+ sensory neurons unlike in wild-type mice

behavior/neurological
• at 7 months
• between 7 and 9 months
• at 7 months, mice exhibit reduced mobility compared with wild-type mice
• between 7 and 9 months, mice exhibit difficulties in movement unlike wild-type mice

limbs/digits/tail
• between 7 and 9 months, mice develop stiffly twisted tails unlike wild-type mice

cellular
• at 9 months in the dorsal root ganglia




Genotype
MGI:6287973
cn7
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6NCrlj * CBA/JNCrlj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Lyz2tm1(cre)Ifo mutation (14 available); any Lyz2 mutation (40 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• mice appear normal at weaning but fail to gain weight

hematopoietic system
• increase in levels of circulating neutrophils
• increase in levels of circulating lymphocytes
• increase in levels of circulating monocytes
• IgG deposition in the glomeruli of kidneys
• macrophages exhibit an acute elevation of proinflammatory cytokines IL-1beta, IL-6, and IP-10, but not IL-10, in response to ingesting dying cells that is not seen in control macrophages
• however, neither bone marrow-derived macrophages nor peritoneal exudate macrophages from 52 week old mice show any defects in the engulfment of dying cells in vitro indicating normal phagocytic capacity

homeostasis/metabolism
• levels of CXCL1, CCL4 and CCL2 are increased in 52-week old mice

immune system
• increase in levels of circulating neutrophils
• increase in levels of circulating lymphocytes
• increase in levels of circulating monocytes
• IgG deposition in the glomeruli of kidneys
• macrophages exhibit an acute elevation of proinflammatory cytokines IL-1beta, IL-6, and IP-10, but not IL-10, in response to ingesting dying cells that is not seen in control macrophages
• however, neither bone marrow-derived macrophages nor peritoneal exudate macrophages from 52 week old mice show any defects in the engulfment of dying cells in vitro indicating normal phagocytic capacity
• levels of CXCL1, CCL4 and CCL2 are increased in 52-week old mice
• mice develop a systemic lupus erythematosus-like disease (SLE)
• increase in serum levels of a broad array of antibodies against autoantigens commonly associated with SLE
• kidneys from aged mice show endocapillary proliferative glomerulonephritis

renal/urinary system
• mice show indications of kidney damage and show increased functional markers of kidney injury
• IgG and complement C1q deposition in the glomeruli of kidneys
• kidneys from aged mice show endocapillary proliferative glomerulonephritis




Genotype
MGI:6151152
cn8
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Cnot3tm1.1Kjkb/Cnot3tm1.1Kjkb
Tg(Ckmm-cre)5Khn/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6NCrlj * CBA/JNCrlj * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Cnot3tm1.1Kjkb mutation (0 available); any Cnot3 mutation (35 available)
Tg(Ckmm-cre)5Khn mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• impaired autophagosome formation

mortality/aging
• mice survive to 7 weeks after birth

cardiovascular system
N
• mice exhibit normal heart weight, cardiac contractility and QT interval

cellular
• impaired autophagosome formation




Genotype
MGI:6151155
cn9
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Cnot3tm1.1Kjkb/Cnot3tm1.1Kjkb
A1cfTg(Myh6-cre/Esr1*)1Jmk/A1cf+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6NCrlj * CBA/JNCrlj * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (5 available); any A1cf mutation (39 available)
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Cnot3tm1.1Kjkb mutation (0 available); any Cnot3 mutation (35 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• tamoxifen-treated mice survive until P40

cardiovascular system
• not as severe as in mice Cnot3tm2.1Tya A1cfTg(Myh6-cre/Esr1*)1Jmk mice

muscle
• not as severe as in mice Cnot3tm2.1Tya A1cfTg(Myh6-cre/Esr1*)1Jmk mice




Genotype
MGI:6151156
cn10
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Cnot3tm1.1Kjkb/Cnot3tm1.1Kjkb
A1cfTg(Myh6-cre/Esr1*)1Jmk/A1cfTg(Myh6-cre/Esr1*)1Jmk
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6NCrlj * CBA/JNCrlj * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (5 available); any A1cf mutation (39 available)
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Cnot3tm1.1Kjkb mutation (0 available); any Cnot3 mutation (35 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• as in mice with one copy of A1cfTg(Myh6-cre/Esr1*)1Jmk

muscle
• as in mice with one copy of A1cfTg(Myh6-cre/Esr1*)1Jmk




Genotype
MGI:5471363
cn11
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
En1tm2(cre)Wrst/En1+
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6NCrlj * CBA/JNCrlj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
En1tm2(cre)Wrst mutation (1 available); any En1 mutation (34 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice show a 76% reduction in survival by 1 year of age
• mice show a 76% reduction in survival by 1 year of age

growth/size/body

behavior/neurological
• mice exhibit tremulousness
• mice show decreased locomotor activity
• mice exhibit a wide-based and ataxic gait

homeostasis/metabolism
• mice exhibit an age dependent decrease in striatal dopamine content in the brain, with a 64.5% reduction by 7-9 months of age compared to controls

nervous system
• while alpha-synuclein inclusions are not seen, accumulation of low-molecular weight alpha-synuclein is seen in the brain
• 60% loss of substantia nigra pars compacta dopamine neurons by 7-9 months of age
• a modest increase in reactive astrocytes in the of substantia nigra pars compacta
• neuronal inclusions are present in the substantia nigra pars compacta
• inclusions are often perinuclear but are also in the neuropil and are positive for ubiquitin
• neuronal inclusions are present in juveniles but are smaller in size than at older ages
• 60% loss of substantia nigra pars compacta dopamine neurons by 7-9 months of age

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Parkinson's disease DOID:14330 OMIM:PS168600
J:192452




Genotype
MGI:5471365
cn12
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Slc6a3tm1(cre)Xz/Slc6a3+
Genetic
Background
involves: 129S1/Sv * C57BL/6NCrlj * CBA/JNCrlj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Slc6a3tm1(cre)Xz mutation (2 available); any Slc6a3 mutation (66 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• mice are more active during the wake cycle than controls at 7 months of age but this difference is no longer significant at 12 months of age

homeostasis/metabolism
• mice exhibit an age dependent decrease in striatal dopamine content in the brain, with a 55.5% reduction by 7-9 months of age compared to controls

nervous system
• 40% loss of substantia nigra pars compacta dopamine neurons by 7-9 months of age
• neuronal inclusions are present in the substantia nigra pars compacta
• inclusions are often perinuclear but are also in the neuropil and are positive for ubiquitin
• neuronal inclusions are present in juveniles but are smaller in size than at older ages
• 40% loss of substantia nigra pars compacta dopamine neurons by 7-9 months of age

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Parkinson's disease DOID:14330 OMIM:PS168600
J:192452




Genotype
MGI:5824126
cn13
Allelic
Composition
Tsc2tm1Djk/Tsc2+
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Camk2a-cre)T29-1Stl/0
Genetic
Background
involves: 129S4/SvJae * BALB/c * C57BL * C57BL/6 * CBA/JNCrlj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Tg(Camk2a-cre)T29-1Stl mutation (2 available)
Tsc2tm1Djk mutation (1 available); any Tsc2 mutation (78 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• in the three-chamber test, mice show impaired preference for sniffing the social target and for social novelty
• during dyadic encounters, mice spend less time sniffing stimulus mice than control littermates

cellular
• mice exhibit high levels of p62/ubiquitin-positive aggregates in cortices at P30, indicating loss of autophagy

nervous system
• between P21 and P29, basal dendrites from layer V A1/S2 pyramidal neurons exhibit more spines than controls, indicating impaired spine pruning, with only 2% of spines pruned
• treatment with rapamycin does not rescue spine pruning

homeostasis/metabolism
• mice exhibit high levels of p62/ubiquitin-positive aggregates in cortices at P30, indicating loss of autophagy




Genotype
MGI:5559516
cn14
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Xbp1tm2Glm/Xbp1tm2Glm
Tg(Defa6-icre)1Rsb/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Tg(Defa6-icre)1Rsb mutation (0 available)
Xbp1tm2Glm mutation (0 available); any Xbp1 mutation (29 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• mice show transmural inflammation as early as 8 weeks of age

digestive/alimentary system
• mice show transmural inflammation as early as 8 weeks of age




Genotype
MGI:5559519
cn15
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Xbp1tm2Glm/Xbp1tm2Glm
Tg(Vil1-cre)997Gum/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * CBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Tg(Vil1-cre)997Gum mutation (2 available)
Xbp1tm2Glm mutation (0 available); any Xbp1 mutation (29 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• with Atg7 and Xbp1 deletion in IECs (intestinal epithelial cells), most mice (>70%) develop discontinuous or transmural inflammation with acute and chronic inflammation ending in an abrupt fashion to muscularis propria and serosa resembling pathologies seen in human patients with Crohn's disease
• enteritis progresses such that it is present in all animals by 18 weeks
• dextran sodium sulfate treatment induces greater inflammation that in wild-type mice
• ileitis is more severe than in animals with IEC deletion of Xbp1 only

cellular

digestive/alimentary system
• intestinal epithelial cells (IECs) completely lack unfolded protein response (UPR)-induced autophagy
• more apoptotic IEC cells are detected than in mice having only Xbp1 deletion in IECs
• with Atg7 and Xbp1 deletion in IECs (intestinal epithelial cells), most mice (>70%) develop discontinuous or transmural inflammation with acute and chronic inflammation ending in an abrupt fashion to muscularis propria and serosa resembling pathologies seen in human patients with Crohn's disease
• enteritis progresses such that it is present in all animals by 18 weeks
• dextran sodium sulfate treatment induces greater inflammation that in wild-type mice
• ileitis is more severe than in animals with IEC deletion of Xbp1 only

homeostasis/metabolism




Genotype
MGI:5824124
cn16
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Camk2a-cre)T29-1Stl/0
Genetic
Background
involves: BALB/c * C57BL * C57BL/6J * C57BL/6NCrlj * CBA/JNCrlj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Tg(Camk2a-cre)T29-1Stl mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• in the three-chamber test, mice show impaired preference for sniffing the social target and for social novelty
• however, mice do not exhibit repetitive behaviors, motor defects, or anxiety-like behaviors
• treatment with rapamycin does not rescue social deficits
• during dyadic encounters, mice spend less time sniffing stimulus mice than control littermates

homeostasis/metabolism
• mice exhibit occasional p62/ubiquitin-positive inclusions in pyramidal neurons at P20 and prominent p62/ubiquitin-positive aggregates in layer II-III and layer V-VI pyramidal neurons at P30, indicating loss of autophagy between P20 and P30 in cortical pyramidal neurons

cellular
• mice exhibit occasional p62/ubiquitin-positive inclusions in pyramidal neurons at P20 and prominent p62/ubiquitin-positive aggregates in layer II-III and layer V-VI pyramidal neurons at P30, indicating loss of autophagy between P20 and P30 in cortical pyramidal neurons

nervous system
• by P29-P30, but not at P19-P20, basal dendrites from layer V A1/S2 pyramidal neurons exhibit more spines than controls, indicating impaired spine pruning, with only 3% of spines pruned between P21 and P29
• treatment with rapamycin does not rescue spine pruning




Genotype
MGI:5470096
cn17
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Tg(SLC18A3-cre)KMisa/0
Genetic
Background
involves: C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Tg(SLC18A3-cre)KMisa mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• mice exhibit normal motor function

nervous system
• with amorphous structures and large inclusions at 2 years of age
• however, there is no loss of motor neurons




Genotype
MGI:6209426
cn18
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Tyr-cre)1Lru/Y
Genetic
Background
involves: C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Tg(Tyr-cre)1Lru mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• cultured primary autophagy-deficient melanocytes stop proliferating after the third passage, unlike autophagy-competent melanocytes which can be maintained up to passage 5
• mice show decreased pigmentation of dorsal hair; melanin content of dorsal hair is reduced by 10-15% relative to that in control mice
• mice exhibit slight hypopigmentation of the tail epidermis
• some melanocytes of tail skin contain misshapen, swollen, and possibly disintegrating mitochondria, not observed in control melanocytes
• however, when cultured in vitro, primary autophagy-deficient melanocytes isolated from body skin of newborn mice show no significant change of melanin content relative to autophagy-competent melanocytes
• pigmentation of the feet is decreased but to a lesser extent than in tail epidermis
• at 9 months of age, pigmentation of tail skin is consistently lower than that of control mice
• melanocyte counts are consistently lower but not significantly decreased in the tail epidermis
• when cultured in vitro, primary autophagy-deficient melanocytes isolated from body skin of newborn mice show increased melanosome-associated vacuolation, unlike autophagy-competent melanocytes
• however, in vivo, both melanocytes and keratinocytes of tail skin contain mature melanosomes, suggesting normal melanosome formation, maturation, and transfer in the absence of an intact autophagy system

integument
• mice show decreased pigmentation of dorsal hair; melanin content of dorsal hair is reduced by 10-15% relative to that in control mice
• mice exhibit slight hypopigmentation of the tail epidermis
• some melanocytes of tail skin contain misshapen, swollen, and possibly disintegrating mitochondria, not observed in control melanocytes
• however, when cultured in vitro, primary autophagy-deficient melanocytes isolated from body skin of newborn mice show no significant change of melanin content relative to autophagy-competent melanocytes
• pigmentation of the feet is decreased but to a lesser extent than in tail epidermis
• at 9 months of age, pigmentation of tail skin is consistently lower than that of control mice
• melanocyte counts are consistently lower but not significantly decreased in the tail epidermis

cellular
• swollen mitochondria are observed in some melanocytes of tail skin, unlike in control mice
• lipidation of microtubule-associated protein 1 light chain 3 beta (LC3), i.e. conversion of LC3-I to LC3-II, is completely blocked, indicating efficient disruption of autophagy in isolated melanocytes; in contrast, both LC3-I and LC3-II are detected in melanocytes of control mice
• cultured primary autophagy-deficient melanocytes stop proliferating after the third passage, unlike autophagy-competent melanocytes which can be maintained up to passage 5
• in culture, primary autophagy-deficient melanocytes show a strong reduction in proliferative capacity and start acquiring senescent morphotypes with distended cytoplasms early in the second passage
• the premature senescent phenotype becomes even more prominent at the end of passage 2 and beginning of passage 3
• autophagy-deficient melanocytes accumulate reactive oxygen species damage, ubiquitinated proteins, and the multi-functional adapter protein SQSTM1/p62

homeostasis/metabolism
• lipidation of microtubule-associated protein 1 light chain 3 beta (LC3), i.e. conversion of LC3-I to LC3-II, is completely blocked, indicating efficient disruption of autophagy in isolated melanocytes; in contrast, both LC3-I and LC3-II are detected in melanocytes of control mice

limbs/digits/tail
• at 9 months of age, pigmentation of tail skin is consistently lower than that of control mice
• melanocyte counts are consistently lower but not significantly decreased in the tail epidermis




Genotype
MGI:6480015
cn19
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Nes-cre)1Kln/0
Wdr45btm1c(EUCOMM)Hmgu/Wdr45btm1c(EUCOMM)Hmgu
Genetic
Background
involves: C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Tg(Nes-cre)1Kln mutation (4 available)
Wdr45btm1c(EUCOMM)Hmgu mutation (0 available); any Wdr45b mutation (13 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• motor deficits at age 4 weeks

nervous system
• many dead cells at age 4 weeks
• many dead cells at age 4 weeks
• severe cerebellar degeneration at age 4 weeks
• many dead Purkinje and granule cells at age 4 weeks
• dense fibrils and severely damaged myelinated nerve fibers in cerebellum at age 4 weeks

growth/size/body
• severe growth retardation of the few mice that are born

mortality/aging
• the few mice that are born die within 4 weeks

cellular
• accumulation of small fragmented and swollen rod-shaped Golgi membranes in cerebellar Purkinje cells at age 4 weeks
• highly enriched smooth ER membranes in cerebellar Purkinje cells and myelinated nerve fibers at age 4 weeks




Genotype
MGI:3590137
cn20
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Mx1-cre)1Cgn/0
Genetic
Background
involves: C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Tg(Mx1-cre)1Cgn mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• disorganization of hepatic lobules and cell swelling
• occasionally observe vacuolated hepatic cells, indicating increased hepatic cell death
• liver fills up most of the abdominal cavity
• Cre- induction leads to increases in liver weight with total liver protein weight being twice that of controls (J:130839)
• hepatocytes lack typical glycogen area, contain aberrant concentric membranous structures that originate form the rough ER and surround various cytoplasmic constituents, and accumulate peroxisomes and deformed mitochondria (J:100199)
• accumulation of ubiquitin-positive inclusions in the cytoplasm (J:100199)
• cytoplasmic inclusion bodies that contain ubiquitinated proteins occur in the hepatocytes of mice expressing Cre (J:130839)
• autophagosome formation in the liver under fasting conditions is not induced in homozygotes
• fasting-induced degradation of cytosolic proteins and mitochondria in the liver does not occur as in controls
• hepatocyte proliferation increases after Cre-induction
• liver function is decreased after Cre-induction with increased levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) apparent in the serum

homeostasis/metabolism
• the hepatocytes of mice expressing Cre have defects in autophagy leading to a build up of cytoplamsic inclusion bodies that contain ubiquitinated proteins
• lower concentration of amino acids in fasted hepatocytes
• leakage of alanine transaminase (J:100199)
• very high levels of AST are found in the sera after Cre-induction due to liver failure (J:130839)
• leakage of alkaline phosphatase (J:100199)
• high levels of ALP are found in the sera after Cre-induction due to liver failure (J:130839)
• leakage of aspartate transaminase (J:100199)
• very high levels of AST are found in the sera after Cre-induction due to liver failure (J:130839)

cellular
• the hepatocytes of mice expressing Cre have defects in autophagy leading to a build up of cytoplamsic inclusion bodies that contain ubiquitinated proteins
• hepatocyte proliferation increases after Cre-induction

growth/size/body
• liver fills up most of the abdominal cavity
• Cre- induction leads to increases in liver weight with total liver protein weight being twice that of controls (J:130839)




Genotype
MGI:3806620
cn21
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Nes-cre)1Wme/0
Genetic
Background
involves: C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Tg(Nes-cre)1Wme mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• the neurons of the cerebral cortex have defects in autophagy leading to a build up of cytoplasmic inclusion bodies that contain ubiquitinated proteins
• these inclusion bodies are visible two days after birth and grow in size and number during development
• increased apoptosis of the neurons occurs in the cerebellar nucleus and the cerebral cortex

homeostasis/metabolism
• the neurons of the cerebral cortex have defects in autophagy leading to a build up of cytoplasmic inclusion bodies that contain ubiquitinated proteins
• these inclusion bodies are visible two days after birth and grow in size and number during development

nervous system
• large pyramidal neurons in the hippocampus are absent
• large pyramidal neurons in the cerebral cortex are absent
• myelinated axons of the cerebellar nuclei are frequently enlarged and contain aberrant membranous structures and degenerated material
• the neurons of the cerebral cortex have defects in autophagy leading to a build up of cytoplasmic inclusion bodies that contain ubiquitinated proteins
• these inclusion bodies are visible two days after birth and grow in size and number during development
• increased apoptosis of the neurons occurs in the cerebellar nucleus and the cerebral cortex

behavior/neurological
• abnormal limb clasping is observed in mice
• is observed




Genotype
MGI:6870515
cn22
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: C57BL/6J * C57BL/6NCrlj * CBA/JNCrlj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Tg(CAG-cre/Esr1*)5Amc mutation (10 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• after 12 h of nutrient deprivation, tamoxifen-treated mouse embryonic fibroblasts (MEFs) fail to show canonical autophagosome formation (punctate LC3 signal), unlike wild-type MEFs

homeostasis/metabolism
• after 12 h of nutrient deprivation, tamoxifen-treated mouse embryonic fibroblasts (MEFs) fail to show canonical autophagosome formation (punctate LC3 signal), unlike wild-type MEFs




Genotype
MGI:5569387
cn23
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Vil1-cre)1000Gum/0
Genetic
Background
involves: C57BL/6J * C57BL/6NCrlj * CBA/JNCrlj * SJL/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Tg(Vil1-cre)1000Gum mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• goblet cells exhibit increased mucin accumulation compared with control cells

cellular
• goblet cells exhibit increased mucin accumulation compared with control cells




Genotype
MGI:5295638
cn24
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Commd10Tg(Vav1-icre)A2Kio/Commd10+
Genetic
Background
involves: C57BL/6NCrlj * C57BL/10 * CBA/Ca * CBA/JNCrlj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Commd10Tg(Vav1-icre)A2Kio mutation (3 available); any Commd10 mutation (24 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• reduction in most myeloid progenitors
• numbers of myeloid subsets CD11b+Gr1- and CD11b-Gr1+ are reduced in blood and decrease further over time
• overall bone marrow cell count is reduced
• common lymphoid progenitors (Lin-Flt3HighIL7RaHighSca-1Lowc-KitLow) are reduced in mutants
• numbers of CCR9+ lymphoid-primed multipotent progenitors are reduced in the bone marrow of mutants
• mutant LSK (Lin-Sca-1+c-Kit+) cells accumulate mitochondria, mitochondrial superoxide, and DNA damage and exhibit increased levels of apoptosis and proliferation
• numbers of hematopoietic stem cells are reduced in all mutants, regardless of disease progression
• absolute numbers of LSK (Lin-Sca-1+c-Kit+) cells significantly increased in asymptomatic 7 week old mutants, however as they develop symptoms, the frequency of LSK cells falls to wild-type levels
• the Lin-Sca-1-c-Kit+ (LK) compartment, containing more mature hematopoietic progenitors, is decreased
• numbers of CD11b+Gr1+ cells are increased in the blood at 5 and 6 weeks of age but then decrease to below wild-type levels at 8 weeks of age
• CD11b+Gr1+ cells in the spleen and bone marrow are increased and show higher proliferation rates
• mutants exhibit presence of atypical myeloid infiltrates in a wide range of organs
• mutants are cytopenic for all blood leukocyte populations except for CD11b+Gr1+ cells
• absolute cell counts of B cells are decreased in the peripheral blood of mutants and numbers drop steadily over time
• immature NK cells (Lin-CD3-CD122+NK1.1+DX5+) are depleted in the bone marrow
• absolute cell counts of NK cells are decreased in the peripheral blood of mutants and numbers drop steadily over time
• absolute cell counts of T cells are decreased in the peripheral blood of mutants and numbers drop steadily over time
• adult bone marrow cells from mutants transplanted together with CD45.1+ wild-type bone marrow cells into lethally irradiated wild-type hosts fail to contribute to reconstitution of cells in the hosts while in noncompetitive reconstitution experiments, lethally irradiated mice die within 4 weeks after transplantation with mutant bone marrow cells, indicating loss of hematopoietic stem cell activity

immune system
• numbers of CD11b+Gr1+ cells are increased in the blood at 5 and 6 weeks of age but then decrease to below wild-type levels at 8 weeks of age
• CD11b+Gr1+ cells in the spleen and bone marrow are increased and show higher proliferation rates
• mutants exhibit presence of atypical myeloid infiltrates in a wide range of organs
• mutants are cytopenic for all blood leukocyte populations except for CD11b+Gr1+ cells
• absolute cell counts of B cells are decreased in the peripheral blood of mutants and numbers drop steadily over time
• immature NK cells (Lin-CD3-CD122+NK1.1+DX5+) are depleted in the bone marrow
• absolute cell counts of NK cells are decreased in the peripheral blood of mutants and numbers drop steadily over time
• absolute cell counts of T cells are decreased in the peripheral blood of mutants and numbers drop steadily over time

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
myelodysplastic syndrome DOID:0050908 OMIM:614286
J:176843




Genotype
MGI:6151162
cn25
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Cnot1tm1Tya/Cnot1tm1Tya
Tg(Ckmm-cre)5Khn/0
Genetic
Background
involves: C57BL/6NCrlj * CBA/JNCrlj * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Cnot1tm1Tya mutation (0 available); any Cnot1 mutation (161 available)
Tg(Ckmm-cre)5Khn mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

cardiovascular system
• not as severe as in Cnot1tm1Tya/Cnot1tm1Tya Tg(Ckmm-cre)5Khn mice
• not as severe as in Cnot1tm1Tya/Cnot1tm1Tya Tg(Ckmm-cre)5Khn mice

muscle
• not as severe as in Cnot1tm1Tya/Cnot1tm1Tya Tg(Ckmm-cre)5Khn mice
• not as severe as in Cnot1tm1Tya/Cnot1tm1Tya Tg(Ckmm-cre)5Khn mice




Genotype
MGI:6480014
cn26
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: C57BL/6NCrlj * CBA/JNCrlj * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• no iron depositions in cerebellum at age 5 weeks

cellular
N
• normal Golgi apparatus morphology in cerebellar Purkinje cells at age 5 weeks
• normal mitochondrial morphology in cerebellum at age 5 weeks
• highly enriched smooth ER membranes in cerebellar Purkinje cells and myelinated nerve fibers at age 5 weeks





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last database update
10/29/2024
MGI 6.24
The Jackson Laboratory