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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Gt(ROSA)26Sortm1.1(CAG-COX8A/Dendra2)Dcc
targeted mutation 1.1, David C Chan
MGI:5318241
Summary 5 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Gt(ROSA)26Sortm1.1(CAG-COX8A/Dendra2)Dcc/Gt(ROSA)26Sortm1.1(CAG-COX8A/Dendra2)Dcc involves: 129S6/SvEvTac * C57BL/6 MGI:5318329
cn2
Gt(ROSA)26Sortm1.1(CAG-COX8A/Dendra2)Dcc/Gt(ROSA)26Sor+
Mfn2tm3Dcc/Mfn2tm3Dcc
Slc6a3tm1.1(cre)Bkmn/Slc6a3+
involves: 129 * 129S6/SvEvTac * C57BL/6J * SJL/J MGI:5441517
cn3
Gt(ROSA)26Sortm1.1(CAG-COX8A/Dendra2)Dcc/Gt(ROSA)26Sor+
Mfn1tm2Dcc/Mfn1tm2Dcc
Slc6a3tm1.1(cre)Bkmn/Slc6a3+
involves: 129 * 129S6/SvEvTac * C57BL/6J * SJL/J MGI:5441518
cn4
Fis1tm1Dcc/Fis1tm1.1Dcc
Gt(ROSA)26Sortm1.1(CAG-COX8A/Dendra2)Dcc/Gt(ROSA)26Sor+
Tg(Stra8-icre)1Reb/0
involves: 129S6/SvEvTac * C57BL/6 * FVB/NJ MGI:6755500
cx5
Gt(ROSA)26Sortm1.1(CAG-COX8A/Dendra2)Dcc/Gt(ROSA)26Sor+
MffGt(AZ0438)Wtsi/MffGt(AZ0438)Wtsi
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * C57BL/6J MGI:7261374


Genotype
MGI:5318329
hm1
Allelic
Composition
Gt(ROSA)26Sortm1.1(CAG-COX8A/Dendra2)Dcc/Gt(ROSA)26Sortm1.1(CAG-COX8A/Dendra2)Dcc
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1.1(CAG-COX8A/Dendra2)Dcc mutation (1 available); any Gt(ROSA)26Sor mutation (764 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• mice are viable and fertile




Genotype
MGI:5441517
cn2
Allelic
Composition
Gt(ROSA)26Sortm1.1(CAG-COX8A/Dendra2)Dcc/Gt(ROSA)26Sor+
Mfn2tm3Dcc/Mfn2tm3Dcc
Slc6a3tm1.1(cre)Bkmn/Slc6a3+
Genetic
Background
involves: 129 * 129S6/SvEvTac * C57BL/6J * SJL/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1.1(CAG-COX8A/Dendra2)Dcc mutation (1 available); any Gt(ROSA)26Sor mutation (764 available)
Mfn2tm3Dcc mutation (2 available); any Mfn2 mutation (22 available)
Slc6a3tm1.1(cre)Bkmn mutation (2 available); any Slc6a3 mutation (55 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants die around 6-7 weeks of age due to malnutrition; this is most likely due to difficulty accessing food and water in normal cages due to a rearing defect
• however, when mutants are supplied with hydrated gel packs and crushed pieces of regular chow, all mutants survive beyond 6 months of age, with a majority surviving past 1 year of age

growth/size/body
• mutants are significantly smaller than controls by 5 weeks of age
• mutants do not gain weight after 4 weeks of age

behavior/neurological
• mutants are hunched by 5 weeks of age
• severe rearing defect as early as 4 weeks of age
• treatment of mutants with L-DOPA alleviates the motor defects
• mutants are hypoactive by 5 weeks of age
• at 4-5 weeks of age, mutants travel only 68% of the distance traveled by wild-type mice and by 8-11 weeks of age, the distance traveled reduces to 34% of wild-type, indicating an age-dependent decline in locomotive activity
• beginning at 4-5 weeks, mutants exhibit progressive bradykinesia
• mutants exhibit a decline in the speed of movement with age compared to controls
• mutants spend twice as much time inactive at 6-7 weeks of age as controls and by 8-11 weeks of age, this increases to 6-fold increase in inactive time

nervous system
• loss of dopaminergic terminals in the striatum, with a 25% reduction in dopaminergic terminals at 3 weeks of age and 76% reduction by 8-10 weeks
• mutants exhibit loss of dopaminergic efferents to the striatum, with a 25% reduction in dopaminergic terminals at 3 weeks of age and a 76% reduction by 8-10 weeks of age
• however, projections to the nucleus accumbens and olfactory tubercle are protected and the dopaminergic terminals are moderately preserved at 11-14 weeks
• dopaminergic neurons remaining have smaller cell bodies and diminished neuronal processes
• dopaminergic neurons exhibit mitochondrial fragmentation and depletion
• retrograde degeneration of substantia nigra pars compacta dopaminergic neurons and to a lesser extent in the mesolimbic pathway
• progressive, retrograde degeneration of dopaminergic neurons in the nigrostriatal circuit, with neuronal loss first seen at 10-12 weeks, when a 52% decrease in TH-positive neurons is seen
• some degeneration is also seen in the mesolimbic pathway, although a lesser extent than in the nigrostriatal circuit
• degeneration of dopaminergic neurons occurs in a stepwise manner, with initial defects at the axon terminals, followed 1-2 months later by degeneration of the cell bodies
• mutants show decreased mitochondrial transport along nerve processes

cellular
• dopaminergic neurons exhibit mitochondrial fragmentation and depletion

skeleton

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Parkinson's disease DOID:14330 OMIM:PS168600
J:188347




Genotype
MGI:5441518
cn3
Allelic
Composition
Gt(ROSA)26Sortm1.1(CAG-COX8A/Dendra2)Dcc/Gt(ROSA)26Sor+
Mfn1tm2Dcc/Mfn1tm2Dcc
Slc6a3tm1.1(cre)Bkmn/Slc6a3+
Genetic
Background
involves: 129 * 129S6/SvEvTac * C57BL/6J * SJL/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1.1(CAG-COX8A/Dendra2)Dcc mutation (1 available); any Gt(ROSA)26Sor mutation (764 available)
Mfn1tm2Dcc mutation (2 available); any Mfn1 mutation (33 available)
Slc6a3tm1.1(cre)Bkmn mutation (2 available); any Slc6a3 mutation (55 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• mice show no abnormal phenotype up to 1 year of age




Genotype
MGI:6755500
cn4
Allelic
Composition
Fis1tm1Dcc/Fis1tm1.1Dcc
Gt(ROSA)26Sortm1.1(CAG-COX8A/Dendra2)Dcc/Gt(ROSA)26Sor+
Tg(Stra8-icre)1Reb/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * FVB/NJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fis1tm1.1Dcc mutation (0 available); any Fis1 mutation (42 available)
Fis1tm1Dcc mutation (0 available); any Fis1 mutation (42 available)
Gt(ROSA)26Sortm1.1(CAG-COX8A/Dendra2)Dcc mutation (1 available); any Gt(ROSA)26Sor mutation (764 available)
Tg(Stra8-icre)1Reb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• no spermatozoa in epididymides
• impaired acrosome development and failure to produce elongated spermatids
• with increased mitochondria content
• 4-fold increase in tubules

cellular
• no spermatozoa in epididymides
• impaired acrosome development and failure to produce elongated spermatids
• with increased mitochondria content
• in round spermatids and giant cells
• in round spermatids and giant cells with aberrant accumulation of autophagic structures
• 4-fold increase in tubules

homeostasis/metabolism
• in round spermatids and giant cells with aberrant accumulation of autophagic structures

endocrine/exocrine glands




Genotype
MGI:7261374
cx5
Allelic
Composition
Gt(ROSA)26Sortm1.1(CAG-COX8A/Dendra2)Dcc/Gt(ROSA)26Sor+
MffGt(AZ0438)Wtsi/MffGt(AZ0438)Wtsi
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1.1(CAG-COX8A/Dendra2)Dcc mutation (1 available); any Gt(ROSA)26Sor mutation (764 available)
MffGt(AZ0438)Wtsi mutation (1 available); any Mff mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• >5% of caudal epididymidal sperm contain kinks in the neck
• >15% of caudal epididymidal sperm contain kinks in the midpiece
• caudal epididymidal sperm show disjointed mitochondrial sheaths with gaps between adjacent organelles
• >40% of caudal epididymidal sperm contain kinks in the principal piece
• >60% of caudal epididymidal sperm contain kinks in the midpiece, principal piece or neck
• most round and elongating spermatids contain tubular mitochondria, unlike in wild-type spermatids where mitochondria are almost always fragmented
• caudal epididymidal sperm are significantly less motile than wild-type sperm
• in an in vitro fertilization assay, cauda epididymidal sperm failed to fertilize any oocytes

cellular
• >5% of caudal epididymidal sperm contain kinks in the neck
• >15% of caudal epididymidal sperm contain kinks in the midpiece
• caudal epididymidal sperm show disjointed mitochondrial sheaths with gaps between adjacent organelles
• >40% of caudal epididymidal sperm contain kinks in the principal piece
• >60% of caudal epididymidal sperm contain kinks in the midpiece, principal piece or neck
• most round and elongating spermatids contain tubular mitochondria, unlike in wild-type spermatids where mitochondria are almost always fragmented
• most round and elongating spermatids contain tubular mitochondria, unlike in wild-type spermatids where mitochondria are almost always fragmented
• total mito-Dendra2 fluorescence is markedly reduced in the midpiece of epididymidal sperm
• caudal epididymidal sperm are significantly less motile than wild-type sperm





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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
06/23/2022
MGI 6.20
The Jackson Laboratory