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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(CAG-EGFP/Map1lc3b)53Nmz
transgene insertion 53, Noboru Mizushima
MGI:3759813
Summary 24 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
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
cn2
Atg5tm1Myok/Atg5tm1Myok
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Tg(Cryaa-cre)10Mlr/0
involves: 129S/SvEv * C57BL/6 * DBA/2 * FVB/N MGI:5529811
cn3
Pik3c3tm1c(EUCOMM)Wtsi/Pik3c3tm1c(EUCOMM)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
involves: C57BL/6 * C57BL/6N * C57BL/6NCrj * DBA MGI:5427446
cn4
Bag3tm1c(EUCOMM)Hmgu/Bag3tm1c(EUCOMM)Hmgu
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Tg(Myhca-cre)1Abel/0
involves: C57BL/6 * C57BL/6N * C57BL/6NCrlj * DBA/2 * FVB/N MGI:6107905
cn5
Pik3c3tm1c(EUCOMM)Wtsi/Pik3c3tm1c(EUCOMM)Wtsi
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
involves: C57BL/6N * C57BL/6NCrj MGI:5427442
cn6
Pik3c3tm1c(EUCOMM)Wtsi/Pik3c3tm1c(EUCOMM)Wtsi
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Tg(Ckmm-cre)5Khn/0
involves: C57BL/6N * C57BL/6NCrj * FVB/N MGI:5427445
cn7
Fis1tm1.1Itl/Fis1tm1.1Itl
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Tg(Ckmm-cre)5Khn/0
involves: C57BL/6NCrlj * C57BL/6NTac * DBA/2 * FVB MGI:6444642
cx8
Becn1tm2.1Blev/Becn1tm2.1Blev
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
involves: 129 * C57BL/6 * C57BL/6J * C57BL/6NCrlj * DBA/2 MGI:6257019
cx9
Atg16l1Gt(BC0122)Wtsi/Atg16l1Gt(BC0122)Wtsi
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
involves: 129P2/OlaHsd * C57BL/6NCrj MGI:5313721
cx10
Atg5tm1Nmz/Atg5tm1Nmz
Tg(CAG-EGFP/Map1lc3b)53Nmz/?
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:3814239
cx11
Tigartm1.2Smat/Tigartm1.2Smat
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6JJcl * C57BL/6NCrj MGI:5319196
cx12
Trp53tm1Tyj/Trp53tm1Tyj
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
involves: 129S2/SvPas * C57BL/6 * C57BL/6NCrj MGI:5319199
cx13
Tsc2tm1Djk/Tsc2+
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
involves: 129S4/SvJae * C57BL/6 * C57BL/6J * C57BL/6NCrlj * DBA/2 MGI:5824122
cx14
Map1stm1.1Lliu/Map1stm1.1Lliu
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
involves: 129S4/SvJaeSor * C57BL/6 * C57BL/6NCrj MGI:4948445
cx15
Atg4dGt(OST254045)Lex/Atg4dGt(OST254045)Lex
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
involves: 129S5/SvEvBrd * C57BL/6J * C57BL/6NCrlj * DBA/2J MGI:6827352
cx16
Bcl2tm1.1Sjk/Bcl2tm1.1Sjk
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
involves: 129X1/SvJ * C57BL/6 * C57BL/6NCrj * SJL MGI:5313437
cx17
Becn1tm1Blev/Becn1+
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
involves: 129X1/SvJ * C57BL/6J * C57BL/6NCrj MGI:3837449
cx18
Dapk1tm1Akc/Dapk1tm1Akc
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
involves: 129X1/SvJ * C57BL/6J * C57BL/6NCrj MGI:4440536
cx19
Becn1tm1Blev/Becn1+
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
involves: 129X1/SvJ * C57BL/6NCrj MGI:5313436
cx20
Rubcnem1Dgre/Rubcnem1Dgre
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
involves: C57BL/6 * C57BL/6J * C57BL/6N * C57BL/6NCrlj * DBA/2 MGI:6196878
cx21
Sox2tm1.2Lan/Sox2tm1.2Lan
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
involves: C57BL/6 * C57BL/6NCrlj * DBA/2 * FVB/N MGI:5572910
cx22
Rubcnem1Dgre/Rubcnem1Dgre
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
involves: C57BL/6 * C57BL/6N * DBA/2 MGI:6287979
cx23
Glipr2em1Blev/Glipr2em1Blev
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
involves: C57BL/6J * DBA/2 MGI:6828762
cx24
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Tg(Myh6-Gsk3b*)19Jusa/0
involves: C57BL/6NCrj * FVB/N MGI:5471802


Genotype
MGI:6287974
cn1
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 (41 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:5529811
cn2
Allelic
Composition
Atg5tm1Myok/Atg5tm1Myok
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Tg(Cryaa-cre)10Mlr/0
Genetic
Background
involves: 129S/SvEv * C57BL/6 * DBA/2 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg5tm1Myok mutation (3 available); any Atg5 mutation (27 available)
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
Tg(Cryaa-cre)10Mlr mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Cataract development in Atg5tm1Myok/Atg5tm1Myok Tg(CAG-EGFP/Map1lc3b)53Nmz/0 Tg(Cryaa-cre)10Mlr/0 mice

homeostasis/metabolism
• absent in lens fiber cells

vision/eye
• absent autophagy in lens fiber cells
• disorganized in the cortical region of aged mice
• however, organelle degradation is normal
• by 6 to 9 months that develops progressively with age
• severe, bilateral at 21 months
• with accumulation of insoluble oxidized proteins and crystallins

cellular
• absent in lens fiber cells




Genotype
MGI:5427446
cn3
Allelic
Composition
Pik3c3tm1c(EUCOMM)Wtsi/Pik3c3tm1c(EUCOMM)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Genetic
Background
involves: C57BL/6 * C57BL/6N * C57BL/6NCrj * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pik3c3tm1c(EUCOMM)Wtsi mutation (1 available); any Pik3c3 mutation (45 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (6 available); any Speer6-ps1 mutation (4 available)
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• livers from fed and starved exhibit blocked autophagy flux compared with control livers

cellular
• livers from fed and starved exhibit blocked autophagy flux compared with control livers

homeostasis/metabolism
• livers from fed and starved exhibit blocked autophagy flux compared with control livers




Genotype
MGI:6107905
cn4
Allelic
Composition
Bag3tm1c(EUCOMM)Hmgu/Bag3tm1c(EUCOMM)Hmgu
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Tg(Myhca-cre)1Abel/0
Genetic
Background
involves: C57BL/6 * C57BL/6N * C57BL/6NCrlj * DBA/2 * FVB/N
Cell Lines HEPD0556_7_B06
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bag3tm1c(EUCOMM)Hmgu mutation (1 available); any Bag3 mutation (31 available)
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
Tg(Myhca-cre)1Abel mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• after 18 hours of starvation, mice exhibit a reduction in LC3-GFP accumulation in the myocardium, indicating suppressed autophagic flux in hearts

homeostasis/metabolism
• after 18 hours of starvation, mice exhibit a reduction in LC3-GFP accumulation in the myocardium, indicating suppressed autophagic flux in hearts




Genotype
MGI:5427442
cn5
Allelic
Composition
Pik3c3tm1c(EUCOMM)Wtsi/Pik3c3tm1c(EUCOMM)Wtsi
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Genetic
Background
involves: C57BL/6N * C57BL/6NCrj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pik3c3tm1c(EUCOMM)Wtsi mutation (1 available); any Pik3c3 mutation (45 available)
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• fed and nutrient-starved conditions mouse embryonic fibroblasts transduced with a cre-expressing adenovirus exhibit blocked autophagy flux unlike control cells

homeostasis/metabolism
• fed and nutrient-starved conditions mouse embryonic fibroblasts transduced with a cre-expressing adenovirus exhibit blocked autophagy flux unlike control cells




Genotype
MGI:5427445
cn6
Allelic
Composition
Pik3c3tm1c(EUCOMM)Wtsi/Pik3c3tm1c(EUCOMM)Wtsi
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Tg(Ckmm-cre)5Khn/0
Genetic
Background
involves: C57BL/6N * C57BL/6NCrj * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pik3c3tm1c(EUCOMM)Wtsi mutation (1 available); any Pik3c3 mutation (45 available)
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
Tg(Ckmm-cre)5Khn mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• hearts from fed and starved exhibit blocked autophagy flux compared with control hearts

cellular
• hearts from fed and starved exhibit blocked autophagy flux compared with control hearts

homeostasis/metabolism
• hearts from fed and starved exhibit blocked autophagy flux compared with control hearts




Genotype
MGI:6444642
cn7
Allelic
Composition
Fis1tm1.1Itl/Fis1tm1.1Itl
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Tg(Ckmm-cre)5Khn/0
Genetic
Background
involves: C57BL/6NCrlj * C57BL/6NTac * DBA/2 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fis1tm1.1Itl mutation (0 available); any Fis1 mutation (47 available)
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
Tg(Ckmm-cre)5Khn mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• increased GFP-LC3 puncta containing mitochondria in the soleus of sedentary mice

homeostasis/metabolism
• increased GFP-LC3 puncta containing mitochondria in the soleus of sedentary mice




Genotype
MGI:6257019
cx8
Allelic
Composition
Becn1tm2.1Blev/Becn1tm2.1Blev
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Genetic
Background
involves: 129 * C57BL/6 * C57BL/6J * C57BL/6NCrlj * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Becn1tm2.1Blev mutation (1 available); any Becn1 mutation (35 available)
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• under fed and resting conditions, mice exhibit a higher number of autophagosomes in skeletal muscle and brain, indicating high basal autophagy

homeostasis/metabolism
• under fed and resting conditions, mice exhibit a higher number of autophagosomes in skeletal muscle and brain, indicating high basal autophagy




Genotype
MGI:5313721
cx9
Allelic
Composition
Atg16l1Gt(BC0122)Wtsi/Atg16l1Gt(BC0122)Wtsi
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6NCrj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg16l1Gt(BC0122)Wtsi mutation (1 available); any Atg16l1 mutation (44 available)
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• reduced exercised-induced autophagy in skeletal muscles compared to in wild-type muscles

homeostasis/metabolism
• reduced exercised-induced autophagy in skeletal muscles compared to in wild-type muscles




Genotype
MGI:3814239
cx10
Allelic
Composition
Atg5tm1Nmz/Atg5tm1Nmz
Tg(CAG-EGFP/Map1lc3b)53Nmz/?
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg5tm1Nmz mutation (1 available); any Atg5 mutation (27 available)
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• E15.5 thymus cells fail to form autophagosomes as occurs in the wild-type fetal thymus

mortality/aging
• neonatal lethality occurs, caused in part by perinatal metabolic process

cellular
• E15.5 thymus cells fail to form autophagosomes as occurs in the wild-type fetal thymus

hematopoietic system
• E15.5 thymus cells fail to form autophagosomes as occurs in the wild-type fetal thymus
• embryonic thymi transplanted under the renal capsule of athymic hosts develop and release CD4 + T cells that mount an autoimmune attack
• this autoimmune attack leads to patches of flaky skin, a massively enlarged colon, atrophy of the uterus, complete absence of fat pads and in many cases enlarged lymph nodes

immune system
• E15.5 thymus cells fail to form autophagosomes as occurs in the wild-type fetal thymus
• embryonic thymi transplanted under the renal capsule of athymic hosts develop and release CD4 + T cells that mount an autoimmune attack
• this autoimmune attack leads to patches of flaky skin, a massively enlarged colon, atrophy of the uterus, complete absence of fat pads and in many cases enlarged lymph nodes

endocrine/exocrine glands
• E15.5 thymus cells fail to form autophagosomes as occurs in the wild-type fetal thymus
• embryonic thymi transplanted under the renal capsule of athymic hosts develop and release CD4 + T cells that mount an autoimmune attack
• this autoimmune attack leads to patches of flaky skin, a massively enlarged colon, atrophy of the uterus, complete absence of fat pads and in many cases enlarged lymph nodes




Genotype
MGI:5319196
cx11
Allelic
Composition
Tigartm1.2Smat/Tigartm1.2Smat
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6JJcl * C57BL/6NCrj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
Tigartm1.2Smat mutation (0 available); any Tigar mutation (54 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• following permanent coronary artery ligation, mice exhibit decreased apoptotic myocyte death and improved cardiac remodeling (smaller fibrotic lesions, decreased cardiac hyperplasia, improved left ventricle size and contractility and decreased accumulation of damaged mitochondria) compared with wild-type mice
• following myocardial infarction
• following myocardial infarction
• following permanent coronary artery ligation, mice exhibit decreased apoptotic myocyte death and improved cardiac remodeling (smaller fibrotic lesions, decreased cardiac hyperplasia, improved left ventricle size and contractility and decreased accumulation of damaged mitochondria) compared with wild-type mice
• following myocardial infarction, cardiac muscles exhibit increased autophagy, levels of reactive oxygen species production mitophagy and decreased mitochondria DNA damage compared to in wild-type mice

cellular
• following myocardial infarction
• following myocardial infarction, cardiac muscles exhibit decreased mitochondria DNA damage compared to in wild-type mice
• however, treatment with chloroquine elevates mitochondria DNA damage to wild-type levels
• following myocardial infarction, autophagy in cardiac muscles is increased compared to in wild-type mice
• following myocardial infarction, cardiac muscles exhibit increased mitophagy compared to in wild-type mice
• however, treatment with chloroquine elevates mitochondrial to wild-type levels
• following myocardial infarction, cardiac muscles exhibit increased levels of reactive oxygen species production compared to in wild-type mice

homeostasis/metabolism
• following permanent coronary artery ligation, mice exhibit decreased apoptotic myocyte death and improved cardiac remodeling (smaller fibrotic lesions, decreased cardiac hyperplasia, improved left ventricle size and contractility and decreased accumulation of damaged mitochondria) compared with wild-type mice
• following myocardial infarction, cardiac muscles exhibit increased autophagy, levels of reactive oxygen species production mitophagy and decreased mitochondria DNA damage compared to in wild-type mice
• following myocardial infarction, autophagy in cardiac muscles is increased compared to in wild-type mice

muscle
• following myocardial infarction
• following myocardial infarction




Genotype
MGI:5319199
cx12
Allelic
Composition
Trp53tm1Tyj/Trp53tm1Tyj
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * C57BL/6NCrj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• following permanent coronary artery ligation, mice exhibit decreased apoptotic myocyte death and improved cardiac remodeling (smaller fibrotic lesions, decreased cardiac hyperplasia, improved left ventricle size and contractility and decreased accumulation of damaged mitochondria) compared with wild-type mice
• following myocardial infarction
• following myocardial infarction
• following permanent coronary artery ligation, mice exhibit decreased apoptotic myocyte death and improved cardiac remodeling (smaller fibrotic lesions, decreased cardiac hyperplasia, improved left ventricle size and contractility and decreased accumulation of damaged mitochondria) compared with wild-type mice
• following myocardial infarction, cardiac muscles exhibit increased autophagy, levels of reactive oxygen species production mitophagy and decreased mitochondria DNA damage compared to in wild-type mice

cellular
• following myocardial infarction
• following myocardial infarction, cardiac muscles exhibit decreased mitochondria DNA damage compared to in wild-type mice
• however, treatment with chloroquine elevates mitochondria DNA damage to wild-type levels
• following myocardial infarction, autophagy in cardiac muscles is increased compared to in wild-type mice
• following myocardial infarction, cardiac muscles exhibit increased mitophagy compared to in wild-type mice
• however, treatment with chloroquine elevates mitochondrial to wild-type levels
• following myocardial infarction, cardiac muscles exhibit increased levels of reactive oxygen species production compared to in wild-type mice

homeostasis/metabolism
• following permanent coronary artery ligation, mice exhibit decreased apoptotic myocyte death and improved cardiac remodeling (smaller fibrotic lesions, decreased cardiac hyperplasia, improved left ventricle size and contractility and decreased accumulation of damaged mitochondria) compared with wild-type mice
• following myocardial infarction, cardiac muscles exhibit increased autophagy, levels of reactive oxygen species production mitophagy and decreased mitochondria DNA damage compared to in wild-type mice
• following myocardial infarction, autophagy in cardiac muscles is increased compared to in wild-type mice

muscle
• following myocardial infarction
• following myocardial infarction




Genotype
MGI:5824122
cx13
Allelic
Composition
Tsc2tm1Djk/Tsc2+
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6J * C57BL/6NCrlj * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
Tsc2tm1Djk mutation (1 available); any Tsc2 mutation (77 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• failure of autophagosome induction in neurons
• rapamycin treatment normalizes autophagosome formation in neurons

homeostasis/metabolism
• failure of autophagosome induction in neurons
• rapamycin treatment normalizes autophagosome formation in neurons




Genotype
MGI:4948445
cx14
Allelic
Composition
Map1stm1.1Lliu/Map1stm1.1Lliu
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Genetic
Background
involves: 129S4/SvJaeSor * C57BL/6 * C57BL/6NCrj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Map1stm1.1Lliu mutation (0 available); any Map1s mutation (35 available)
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• starved neonates survival time is half that of similarly treated wild-type mice

cellular
• heart and liver tissues from pups under nutritive stress exhibit early accumulation of autophagosomes associated with impaired autophagosomal degradation compared with tissues form wild-type mice

homeostasis/metabolism
• heart and liver tissues from pups under nutritive stress exhibit early accumulation of autophagosomes associated with impaired autophagosomal degradation compared with tissues form wild-type mice




Genotype
MGI:6827352
cx15
Allelic
Composition
Atg4dGt(OST254045)Lex/Atg4dGt(OST254045)Lex
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Genetic
Background
involves: 129S5/SvEvBrd * C57BL/6J * C57BL/6NCrlj * DBA/2J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg4dGt(OST254045)Lex mutation (1 available); any Atg4d mutation (18 available)
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• misaligned and reduced size cell body with abnormally shaped nucleus and high numbers of autophagosomes
• abnormal at 2 months persisting at 5 months
• with reactive gliosis and synaptic clusters of GABA-A receptors
• in the cerebellar molecular layer
• age-dependent cerebellar neurodegeneration
• in aged mice without increased apoptosis

behavior/neurological
• at 2 and 5 months, more pronounced with age
• cerebellar ataxia
• at 2 and 5 months of age on a rotarod and balance beam, more pronounced with age
• at 2 and 5 months, more pronounced with age
• at 2 and 5 months, more pronounced with age

homeostasis/metabolism
• increased and smaller size GFP-LC3B+ structures in mouse embryonic fibroblasts
• increased ATG8-like proteins in GFP-LCB3 puncta in the liver, heart, and skeletal muscle of mice fed ad libitum or after 24 h fast
• however, autophagy flux is normal

cellular
• increased and smaller size GFP-LC3B+ structures in mouse embryonic fibroblasts
• increased ATG8-like proteins in GFP-LCB3 puncta in the liver, heart, and skeletal muscle of mice fed ad libitum or after 24 h fast
• however, autophagy flux is normal




Genotype
MGI:5313437
cx16
Allelic
Composition
Bcl2tm1.1Sjk/Bcl2tm1.1Sjk
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6 * C57BL/6NCrj * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bcl2tm1.1Sjk mutation (1 available); any Bcl2 mutation (41 available)
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• decreased exercise endurance
• reduced in starved mouse embryonic fibroblasts and skeletal and cardiac muscles or skeletal muscles from exercised mice
• however, basal levels of autophagy are normal
• in mice fed a high-fat diet with no drop in levels following exercise unlike in wild-type mice
• exercised mice fed a high-fat diet fail to exhibit an increase in carbon dioxide production unlike wild-type mice
• exercised mice fed a high-fat diet fail to exhibit an increase in oxygen consumption unlike wild-type mice
• mice exhibit impaired exercise-induced increase in insulin sensitivity compared with wild-type mice
• exercised mice fail to exhibit a decrease in circulating glucose levels compared with wild-type mice
• exercised mice exhibit less of a reduction in plasma insulin levels compared with wild-type mice
• exercised mice fed a high-fat diet fail to exhibit protection from impaired glucose tolerance compared with wild-type mice
• however, mice fed standard chow exhibit normal glucose tolerance
• exercised mice fed a high-fat diet fail to exhibit an increase in adiponectin levels unlike in wild-type mice
• exercised mice fed a high-fat diet exhibit less of a decrease in cholesterol levels compared with wild-type mice
• exercised mice fed a high-fat diet exhibit less of a decrease in triglyceride levels compared with wild-type mice
• exercised mice fed a high-fat diet fail to exhibit an increase in heat production unlike wild-type mice

cellular
• reduced in starved mouse embryonic fibroblasts and skeletal and cardiac muscles or skeletal muscles from exercised mice
• however, basal levels of autophagy are normal
• impaired in exercised mice

adipose tissue
• exercised mice fed a high-fat diet exhibit less of a decrease in percent fat mass compared with wild-type mice

muscle
N
• baseline cardiac and skeletal muscle properties are normal
• impaired in exercised mice

behavior/neurological
• decreased exercise endurance




Genotype
MGI:3837449
cx17
Allelic
Composition
Becn1tm1Blev/Becn1+
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6J * C57BL/6NCrj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Becn1tm1Blev mutation (1 available); any Becn1 mutation (35 available)
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• mutants show decreased autophagy during starvation conditions in muscle and bronchial epithelial cells

homeostasis/metabolism
• mutants show decreased autophagy during starvation conditions in muscle and bronchial epithelial cells




Genotype
MGI:4440536
cx18
Allelic
Composition
Dapk1tm1Akc/Dapk1tm1Akc
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6J * C57BL/6NCrj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dapk1tm1Akc mutation (0 available); any Dapk1 mutation (125 available)
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• inhibited GFP-LC3 dots accumulation in embryonic fibroblasts (MEFs)
• reduced number of GFP-LC3 dots/mm2 in MEFs treated with thapsigargin for 24 h




Genotype
MGI:5313436
cx19
Allelic
Composition
Becn1tm1Blev/Becn1+
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6NCrj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Becn1tm1Blev mutation (1 available); any Becn1 mutation (35 available)
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• reduced exercised-induced autophagy in skeletal muscles compared to in wild-type muscles

homeostasis/metabolism
• mice exhibit decreased maximal treadmill running distance compared with wild-type mice
• reduced exercised-induced autophagy in skeletal muscles compared to in wild-type muscles

behavior/neurological
• mice exhibit decreased maximal treadmill running distance compared with wild-type mice




Genotype
MGI:6196878
cx20
Allelic
Composition
Rubcnem1Dgre/Rubcnem1Dgre
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Genetic
Background
involves: C57BL/6 * C57BL/6J * C57BL/6N * C57BL/6NCrlj * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rubcnem1Dgre mutation (1 available); any Rubcn mutation (39 available)
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• increased numbers of LC3 (Map1lc3) puncta
• unable to translocate LC3 (Map1lc3) to LAP (LC3-associated phagocytosis)-engaged phagosome
• phagocytosis

immune system
• increased numbers of LC3 (Map1lc3) puncta
• unable to translocate LC3 (Map1lc3) to LAP (LC3-associated phagocytosis)-engaged phagosome
• phagocytosis




Genotype
MGI:5572910
cx21
Allelic
Composition
Sox2tm1.2Lan/Sox2tm1.2Lan
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Genetic
Background
involves: C57BL/6 * C57BL/6NCrlj * DBA/2 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sox2tm1.2Lan mutation (0 available); any Sox2 mutation (56 available)
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• impaired in embryonic cells

homeostasis/metabolism
• impaired in embryonic cells




Genotype
MGI:6287979
cx22
Allelic
Composition
Rubcnem1Dgre/Rubcnem1Dgre
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Genetic
Background
involves: C57BL/6 * C57BL/6N * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rubcnem1Dgre mutation (1 available); any Rubcn mutation (39 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 acutely increased in mice injected with UV-irradiated dying thymocytes
• serum IL-1beta levels are acutely 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 acutely 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 acutely increased in mice injected with UV-irradiated dying thymocytes
• serum IL-1beta levels are acutely 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 acutely increased in mice injected with UV-irradiated dying thymocytes




Genotype
MGI:6828762
cx23
Allelic
Composition
Glipr2em1Blev/Glipr2em1Blev
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Genetic
Background
involves: C57BL/6J * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Glipr2em1Blev mutation (0 available); any Glipr2 mutation (36 available)
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• increased autophagosomes in all tissues examined, including heart, liver, and skeletal muscle due to increased autophagic flux
• however, autophagosome maturation is normal

homeostasis/metabolism
• increased autophagosomes in all tissues examined, including heart, liver, and skeletal muscle due to increased autophagic flux
• however, autophagosome maturation is normal




Genotype
MGI:5471802
cx24
Allelic
Composition
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Tg(Myh6-Gsk3b*)19Jusa/0
Genetic
Background
involves: C57BL/6NCrj * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (5 available)
Tg(Myh6-Gsk3b*)19Jusa mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• following 2 hours of ischemia without reperfusion
• however, treatment with rapamycin reduces infarct size

cellular
• reduced autophagy in the heart following 2 hours of ischemia or ischemia with reperfusion
• however, treatment with rapamycin restores autophagy in both cases

homeostasis/metabolism
• following 2 hours of ischemia without reperfusion
• however, treatment with rapamycin reduces infarct size
• reduced autophagy in the heart following 2 hours of ischemia or ischemia with reperfusion
• however, treatment with rapamycin restores autophagy in both cases





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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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last database update
04/23/2024
MGI 6.23
The Jackson Laboratory