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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Atg5tm1Myok
targeted mutation 1, Minesuke Yokoyama
MGI:3663625
Summary 15 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Atg5tm1Myok/Atg5tm1Myok involves: 129S/SvEv MGI:5784717
hm2
Atg5tm1Myok/Atg5tm1Myok involves: 129S/SvEv * C57BL/6 MGI:3713119
cn3
Atg5tm1Myok/Atg5tm1Myok
Myl2tm1(cre)Krc/Myl2+
involves: 129S/SvEv * 129S4/SvJae MGI:3713112
cn4
Atg5tm1Myok/Atg5tm1Myok
Tg(CAG-cre)13Miya/?
involves: 129S/SvEv * C57BL/6 MGI:3713121
cn5
Atg5tm1Myok/Atg5tm1Myok
Tg(Mx1-cre)1Cgn/?
involves: 129S/SvEv * C57BL/6 * CBA MGI:3713122
cn6
Atg5tm1Myok/Atg5tm1Myok
Tg(Kap-cre)1Isa/0
involves: 129S/SvEv * C57BL/6 * DBA MGI:5306237
cn7
Atg5tm1Myok/Atg5tm1Myok
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
Tg(Cryaa-cre)10Mlr/0
involves: 129S/SvEv * C57BL/6 * DBA/2 * FVB/N MGI:5529811
cn8
Atg5tm1Myok/Atg5tm1Myok
Tg(Pomc1-cre)1Gsb/0
involves: 129S/SvEv * C57BL/6 * FVB/N MGI:5784718
cn9
Atg5tm1Myok/Atg5tm1Myok
Tg(Myh6-cre)2182Mds/?
involves: 129S/SvEv * C57BL/6 * FVB/N MGI:3713114
cn10
Atg5tm1Myok/Atg5tm1Myok
Tg(BEST1-cre)1Taf/0
involves: 129S/SvEv * C57BL/6J MGI:5554206
cn11
Atg5tm1Myok/Atg5tm1Myok
Rhebtm1.1Otsu/Rhebtm1.1Otsu
Tg(Myh6-cre)2182Mds/0
involves: 129S/SvEv * C57BL/6J * FVB/N MGI:5502749
cn12
Atg5tm1Myok/Atg5tm1Myok
Tg(Vil1-cre)1000Gum/0
involves: 129S/SvEv * C57BL/6J * SJL/J MGI:5569384
cn13
Atg5tm1Myok/Atg5tm1Myok
Tg(Vil1-cre)997Gum/0
involves: 129S/SvEv * C57BL/6 * SJL MGI:3818605
cn14
Atg5tm1Myok/Atg5tm1Myok
Tg(Nes-cre)1Kln/?
involves: 129S/SvEv * C57BL/6 * SJL MGI:3713123
cn15
Atg5tm1Myok/Atg5tm1Myok
A1cfTg(Myh6-cre/Esr1*)1Jmk/?
involves: 129S/SvEv * FVB/N MGI:3713115


Genotype
MGI:5784717
hm1
Allelic
Composition
Atg5tm1Myok/Atg5tm1Myok
Genetic
Background
involves: 129S/SvEv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg5tm1Myok mutation (2 available); any Atg5 mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
N
• mice exhibit normal autophagy in the hypothalamus




Genotype
MGI:3713119
hm2
Allelic
Composition
Atg5tm1Myok/Atg5tm1Myok
Genetic
Background
involves: 129S/SvEv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg5tm1Myok mutation (2 available); any Atg5 mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• mice are normal




Genotype
MGI:3713112
cn3
Allelic
Composition
Atg5tm1Myok/Atg5tm1Myok
Myl2tm1(cre)Krc/Myl2+
Genetic
Background
involves: 129S/SvEv * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg5tm1Myok mutation (2 available); any Atg5 mutation (18 available)
Myl2tm1(cre)Krc mutation (3 available); any Myl2 mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die after thoracic transverse aortic constriction of heart failure

cardiovascular system
• 1 week following thoracic transverse aortic constriction (TAC) or a 7 day treatment with isoproterenol left ventricular dilation is observed
• thoracic transverse aortic constriction (TAC) and isoproterenol induce severe cardiac dysfunction
• 4 weeks following TAC

homeostasis/metabolism
• following a 7 day treatment with isoproterenol the left ventricle is dilated and mice exhibit severe cardiac dysfuction, unlike wild-type mice where the treatment has no significant effect




Genotype
MGI:3713121
cn4
Allelic
Composition
Atg5tm1Myok/Atg5tm1Myok
Tg(CAG-cre)13Miya/?
Genetic
Background
involves: 129S/SvEv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg5tm1Myok mutation (2 available); any Atg5 mutation (18 available)
Tg(CAG-cre)13Miya mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• diffuse cytoplasmic signals and inclusions are found in the liver




Genotype
MGI:3713122
cn5
Allelic
Composition
Atg5tm1Myok/Atg5tm1Myok
Tg(Mx1-cre)1Cgn/?
Genetic
Background
involves: 129S/SvEv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg5tm1Myok mutation (2 available); any Atg5 mutation (18 available)
Tg(Mx1-cre)1Cgn mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• few inclusions form immediately following injection of inosinic acid-polycytidylic acid (pIpC) but large ubiquitin-positive inclusions are present 16 days post-injection




Genotype
MGI:5306237
cn6
Allelic
Composition
Atg5tm1Myok/Atg5tm1Myok
Tg(Kap-cre)1Isa/0
Genetic
Background
involves: 129S/SvEv * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg5tm1Myok mutation (2 available); any Atg5 mutation (18 available)
Tg(Kap-cre)1Isa mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• increased excretion of most amino acids, with significant increases in threonine, tryptophan, valine, and alanine excretion is observed in 6-month old mice
• mice exhibit mild glycosuria at 6 months of age
• at 8 weeks of age, (left) kidney weight-to-body weight is slight increased relative to littermate controls
• at 8 weeks, slight tubular cell hypertrophy is observed but interstitial nephritis or fibrosis is not apparent; accumulation of numerous crescent membranous structures in tubular epithelial cells, primarily adjacent to mitochondria is present at 6 weeks with accumulation of similar (smaller) structures observed at 9 months
• deformed mitochondria are found in tubular cells of mutants but not in controls
• accumulation of cytosolic amorphous substrates in proximal tubular cells is apparent at 6 months
• massive accumulation of p62- and ubiquitin-positive inclusion bodies is observed almost exclusively in proximal tubules at 9 months

mortality/aging
N
• all mice survive during observational period (<9 months)

homeostasis/metabolism
N
• no albuminuria or increased blood urea nitrogen level is observed in mice up to 9 months of age compared to littermate controls
• no phosphaturia is observed
• increased excretion of most amino acids, with significant increases in threonine, tryptophan, valine, and alanine excretion is observed in 6-month old mice
• mice exhibit mild glycosuria at 6 months of age

cellular
• in kidney cortex homogenates from 8-week old mice, conversion of microtubule-associated protein 1 light chain 3 (LC3-I) to LC3-II is suppressed, indicative of defective autophagy
• after ischemia-reperfusion injury, severely injured tubules with accumulation of tubular sediments and vacuolation in the cortex are observed, whereas injury severity is reduced in injured controls; conversion of LC-I to LC-II in cortex as measured by Western blot is significantly suppressed indicating autophagy deficiency




Genotype
MGI:5529811
cn7
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 (2 available); any Atg5 mutation (18 available)
Tg(CAG-EGFP/Map1lc3b)53Nmz mutation (4 available)
Tg(Cryaa-cre)10Mlr mutation (0 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

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:5784718
cn8
Allelic
Composition
Atg5tm1Myok/Atg5tm1Myok
Tg(Pomc1-cre)1Gsb/0
Genetic
Background
involves: 129S/SvEv * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg5tm1Myok mutation (2 available); any Atg5 mutation (18 available)
Tg(Pomc1-cre)1Gsb mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• complete loss of autophagy in hypothalamus neurons whether mice are fed a normal or high-fat diet

adipose tissue
N
• mice fed a normal diet exhibit normal fat mass and adiposity

growth/size/body
N
• mice fed standard chow exhibit normal body weight, lean mass and body length
• mice fed a high-fat diet exhibit normal body weight gain

nervous system
N
• mice exhibit normal POMC neuron numbers and corticotroph function




Genotype
MGI:3713114
cn9
Allelic
Composition
Atg5tm1Myok/Atg5tm1Myok
Tg(Myh6-cre)2182Mds/?
Genetic
Background
involves: 129S/SvEv * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg5tm1Myok mutation (2 available); any Atg5 mutation (18 available)
Tg(Myh6-cre)2182Mds mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• mice are normal




Genotype
MGI:5554206
cn10
Allelic
Composition
Atg5tm1Myok/Atg5tm1Myok
Tg(BEST1-cre)1Taf/0
Genetic
Background
involves: 129S/SvEv * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg5tm1Myok mutation (2 available); any Atg5 mutation (18 available)
Tg(BEST1-cre)1Taf mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
vision/eye
N
• at 12 weeks of age, ERG responses are not different from wild-type littermate controls
• no significant loss of nuclei in the outer nuclear layer by 24 weeks through 1.5 years of age
• when control and mutant mice received an i.p. injection of 9-cis retinal and then were dark-adapted for 24 hours, scotopic and photopic electroretinogram recordings showed no significant differences in rod and cone function
• rod responses to bright-light stimuli are decreased at 16 weeks compared to controls
• cone responses to bright-light stimuli are decreased at 16 weeks compared to controls

cellular
• in retina pigmented epithelium (RPE) cells of mutants, degenerating phagosomes with undigested photoreceptor outer segment (POS) material are observed in contrast to controls where POS are in single-membrane phagosomes




Genotype
MGI:5502749
cn11
Allelic
Composition
Atg5tm1Myok/Atg5tm1Myok
Rhebtm1.1Otsu/Rhebtm1.1Otsu
Tg(Myh6-cre)2182Mds/0
Genetic
Background
involves: 129S/SvEv * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg5tm1Myok mutation (2 available); any Atg5 mutation (18 available)
Rhebtm1.1Otsu mutation (0 available); any Rheb mutation (16 available)
Tg(Myh6-cre)2182Mds mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging




Genotype
MGI:5569384
cn12
Allelic
Composition
Atg5tm1Myok/Atg5tm1Myok
Tg(Vil1-cre)1000Gum/0
Genetic
Background
involves: 129S/SvEv * C57BL/6J * SJL/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg5tm1Myok mutation (2 available); any Atg5 mutation (18 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
• however, the number of goblet cells is normal and hydrogen peroxide treatment normalizes mucin levels




Genotype
MGI:3818605
cn13
Allelic
Composition
Atg5tm1Myok/Atg5tm1Myok
Tg(Vil1-cre)997Gum/0
Genetic
Background
involves: 129S/SvEv * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg5tm1Myok mutation (2 available); any Atg5 mutation (18 available)
Tg(Vil1-cre)997Gum mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• aberrant, disorganized granules as well as decreased granule numbers are observed in these mice
• virtually all Paneth cells have lysozyme localized throughout the cell instead of being discretely packaged within vesicles
• Paneth cells also have degenerating mitochondria, loss of granules and the frequent absence of apical microvilli
• adjacent crypt lumen often contains intact Paneth granules and cytoplasm, which is a phenomenon not observed in wild-type controls

cellular
• autophagy by the ileal epithelium is severely reduced in these mice

endocrine/exocrine glands
• aberrant, disorganized granules as well as decreased granule numbers are observed in these mice
• virtually all Paneth cells have lysozyme localized throughout the cell instead of being discretely packaged within vesicles
• Paneth cells also have degenerating mitochondria, loss of granules and the frequent absence of apical microvilli
• adjacent crypt lumen often contains intact Paneth granules and cytoplasm, which is a phenomenon not observed in wild-type controls




Genotype
MGI:3713123
cn14
Allelic
Composition
Atg5tm1Myok/Atg5tm1Myok
Tg(Nes-cre)1Kln/?
Genetic
Background
involves: 129S/SvEv * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg5tm1Myok mutation (2 available); any Atg5 mutation (18 available)
Tg(Nes-cre)1Kln mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• some mice die after 3 weeks

nervous system
• ubiquitin-positive inclusions are found in the thalamus pon, medulla, dorsal root ganglion, midbrain, cerebral cortex, hippocampus (especially in CA3 and CA4), striatum and olfactory bulb autophagosomes formation in the brain is impaired
• axonal swelling in the posterior thalamic nucleus
• loss of pyramidal cells in the cerebral cortex
• apoptosis is detected in granular cells
• axonal swelling in the cerebral cortex, nucleus gracilis, posterior thalamic nucleus, hippocampus, inferior colliculus, tricaudal pons and reticular nucleus
• however, few degenerating Purkinje cells exhibit inclusions
• ubiquitin-positive inclusions are found in the thalamus pon, medulla, dorsal root ganglion, midbrain, cerebral cortex, hippocampus (especially in CA3 and CA4), striatum and olfactory bulb
• inclusions are time-dependent and are more limited in newborns than in adults

behavior/neurological
• progressive motor and behavioral deficits after three weeks of age
• progressive motor deficits after three weeks of age including ataxia and a decrease in mean stride length
• when suspended by their tails
• at 12 weeks
• coordination, balance and grip strength are impaired in a rotarod and wire hang task
• grip strength is impaired in a rotarod and wire hang task

cellular
• autophagosomes formation in the brain is impaired

growth/size/body
• body weight is about 1.5-times lower than that of wild-type




Genotype
MGI:3713115
cn15
Allelic
Composition
Atg5tm1Myok/Atg5tm1Myok
A1cfTg(Myh6-cre/Esr1*)1Jmk/?
Genetic
Background
involves: 129S/SvEv * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Atg5tm1Myok mutation (2 available); any Atg5 mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• cardiomyocyte fiber cross-sectional area is increased following tamoxifen treatment
• however, cardiomyocyte fibers are otherwise normal
• increase in the heart to body weight ratio following tamoxifen treatment
• following tamoxifen treatment
• following tamoxifen treatment
• calcium cycling is impaired following tamoxifen treatment
• decrease in the autophagy levels following tamoxifen treatment

respiratory system
• increase in the lung to body weight ratio following tamoxifen treatment

muscle
• cardiomyocyte fiber cross-sectional area is increased following tamoxifen treatment
• however, cardiomyocyte fibers are otherwise normal
• following tamoxifen treatment





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last database update
11/22/2016
MGI 6.06
The Jackson Laboratory