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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Gt(ROSA)26Sortm1Lrsn
targeted mutation 1, Nils-Goran Larsson
MGI:5292496
Summary 6 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Gt(ROSA)26Sortm1Lrsn/Gt(ROSA)26Sor+
Park2tm1Roo/Park2tm1Roo
Slc6a3tm1(cre)Lrsn/Slc6a3+
Tfamtm1Lrsn/Tfamtm1Lrsn
involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6 MGI:5292517
cn2
Gt(ROSA)26Sortm1Lrsn/Gt(ROSA)26Sor+
Mfn2tm1.1Arte/Mfn2tm1.1Arte
Slc6a3tm1(cre)Lrsn/Slc6a3+
involves: 129S1/Sv * 129X1/SvJ MGI:5440842
cn3
Gt(ROSA)26Sortm1Lrsn/Gt(ROSA)26Sor+
Slc6a3tm1(cre)Lrsn/Slc6a3+
Tfamtm1Lrsn/Tfamtm1Lrsn
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:5292515
cn4
Afg3l2tm1Arte/Afg3l2tm1Arte
Gt(ROSA)26Sortm1Lrsn/Gt(ROSA)26Sor+
Tg(Pcp2-cre)2Mpin/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:5476802
cn5
Afg3l2tm1Arte/Afg3l2tm1Arte
Gt(ROSA)26Sortm1Lrsn/Gt(ROSA)26Sor+
Tg(Plp1-cre/ERT)3Pop/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J MGI:5817781
cn6
Afg3l1tm1.1Arte/Afg3l1tm1.1Arte
Afg3l2tm1Arte/Afg3l2tm1Arte
Gt(ROSA)26Sortm1Lrsn/Gt(ROSA)26Sor+
Tg(Plp1-cre/ERT)3Pop/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * C57BL/6N MGI:5817784


Genotype
MGI:5292517
cn1
Allelic
Composition
Gt(ROSA)26Sortm1Lrsn/Gt(ROSA)26Sor+
Park2tm1Roo/Park2tm1Roo
Slc6a3tm1(cre)Lrsn/Slc6a3+
Tfamtm1Lrsn/Tfamtm1Lrsn
Genetic
Background
involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Lrsn mutation (0 available); any Gt(ROSA)26Sor mutation (364 available)
Park2tm1Roo mutation (0 available); any Park2 mutation (20 available)
Slc6a3tm1(cre)Lrsn mutation (0 available); any Slc6a3 mutation (38 available)
Tfamtm1Lrsn mutation (0 available); any Tfam mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• YFP+ neurons exhibit one or more grossly enlarged, rounded mitochondria in the perinuclear region of the soma and in proximal segment of dendrites with some cells containing fragmented mitochondria and small, spherical mitochondrial clustered around the nucleus
• YFP+ neurons exhibit a progressive reduction in distal axonal mitochondrial numbers compared with control cells
• however, mitochondria in the distal dopamine axons are morphologically spared
• neurons exhibit less intense staining with a retrograde tracer (fluorogold) suggesting impaired retrograde transport and/or uptake of the tracer compared with control cells




Genotype
MGI:5440842
cn2
Allelic
Composition
Gt(ROSA)26Sortm1Lrsn/Gt(ROSA)26Sor+
Mfn2tm1.1Arte/Mfn2tm1.1Arte
Slc6a3tm1(cre)Lrsn/Slc6a3+
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Lrsn mutation (0 available); any Gt(ROSA)26Sor mutation (364 available)
Mfn2tm1.1Arte mutation (0 available); any Mfn2 mutation (17 available)
Slc6a3tm1(cre)Lrsn mutation (0 available); any Slc6a3 mutation (38 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• profound reduction in the number of labeled mitochondria in the dorsal striatum
• mitochondria are spherical and enlarged with disorganized cristae

cellular
• mitochondria in dopaminergic neurons are spherical and enlarged with disorganized cristae
• profound reduction in the number of labeled mitochondria in the dorsal striatum
• mitochondria in dopaminergic neurons are spherical and enlarged with disorganized cristae




Genotype
MGI:5292515
cn3
Allelic
Composition
Gt(ROSA)26Sortm1Lrsn/Gt(ROSA)26Sor+
Slc6a3tm1(cre)Lrsn/Slc6a3+
Tfamtm1Lrsn/Tfamtm1Lrsn
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Lrsn mutation (0 available); any Gt(ROSA)26Sor mutation (364 available)
Slc6a3tm1(cre)Lrsn mutation (0 available); any Slc6a3 mutation (38 available)
Tfamtm1Lrsn mutation (0 available); any Tfam mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Mitochondria abnormalities in Tfamtm1Lrsn/Tfamtm1Lrsn Slc6a3tm1(cre)Lrsn/Slc6a3+ Gt(ROSA)26Sortm1Lrsn/Gt(ROSA)26Sor+ neurons

nervous system
• YFP+ neurons exhibit one or more grossly enlarged, rounded mitochondria in the perinuclear region of the soma and in proximal segment of dendrites with some cells containing fragmented mitochondria and small, spherical mitochondrial clustered around the nucleus
• YFP+ neurons exhibit a progressive reduction in distal axonal mitochondrial numbers compared with control cells

cellular
• smaller mitochondrial and the largest aggregates in a rare number of neurons exhibit reduced import competence compared with mitochondria in control cells

behavior/neurological
• impaired from 20 weeks of age

growth/size/body
• from 20 weeks of age

muscle
• rigidity from 20 weeks of age




Genotype
MGI:5476802
cn4
Allelic
Composition
Afg3l2tm1Arte/Afg3l2tm1Arte
Gt(ROSA)26Sortm1Lrsn/Gt(ROSA)26Sor+
Tg(Pcp2-cre)2Mpin/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Afg3l2tm1Arte mutation (0 available); any Afg3l2 mutation (17 available)
Gt(ROSA)26Sortm1Lrsn mutation (0 available); any Gt(ROSA)26Sor mutation (364 available)
Tg(Pcp2-cre)2Mpin mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Abnormal mitochondrial network in Afg3l2tm1Arte/Afg3l2tm1Arte Tg(Pcp2-cre)2Mpin/0 Gt(ROSA)26Sortm1Lrsn/Gt(ROSA)26Sor+ mice

nervous system
• at 4 weeks, Purkinje cells exhibit fragmentation of mitochondria unlike control cells
• at 6 weeks, mitochondrial fragmentation is very pronounced
• Purkinje cell electrophysiological properties are normal at 4 to 5 weeks of age




Genotype
MGI:5817781
cn5
Allelic
Composition
Afg3l2tm1Arte/Afg3l2tm1Arte
Gt(ROSA)26Sortm1Lrsn/Gt(ROSA)26Sor+
Tg(Plp1-cre/ERT)3Pop/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Afg3l2tm1Arte mutation (0 available); any Afg3l2 mutation (17 available)
Gt(ROSA)26Sortm1Lrsn mutation (0 available); any Gt(ROSA)26Sor mutation (364 available)
Tg(Plp1-cre/ERT)3Pop mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• at 8 weeks of age, oligodendrocytes in the corpus callosum of tamoxifen-treated mice exhibit fragmented mitochondria, unlike in control mice
• at 8 weeks of age, oligodendrocytes in the corpus callosum of tamoxifen-treated mice exhibit swollen mitochondria, unlike in control mice




Genotype
MGI:5817784
cn6
Allelic
Composition
Afg3l1tm1.1Arte/Afg3l1tm1.1Arte
Afg3l2tm1Arte/Afg3l2tm1Arte
Gt(ROSA)26Sortm1Lrsn/Gt(ROSA)26Sor+
Tg(Plp1-cre/ERT)3Pop/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * C57BL/6N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Afg3l1tm1.1Arte mutation (0 available); any Afg3l1 mutation (19 available)
Afg3l2tm1Arte mutation (0 available); any Afg3l2 mutation (17 available)
Gt(ROSA)26Sortm1Lrsn mutation (0 available); any Gt(ROSA)26Sor mutation (364 available)
Tg(Plp1-cre/ERT)3Pop mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• at 10 weeks of age, tamoxifen-treated mice show a strong reduction of mt-YFP+ melanoblasts in the outer root sheath of the hair follicle
• at 28 weeks of age, pigmented hair follicles and c-KIT+ melanoblasts are significantly reduced in dorsal skin, suggesting that premature hair greying is caused by progressive loss of melanoblasts that share a common developmental origin with Schwann cells
• tamoxifen-treated mice show progressive and rapid loss of targeted (mt-YFP+) oligodendrocytes in the corpus callosum after 6 weeks of age, with only a few targeted cells remaining at 28 weeks
• at 10 weeks, the number of total APC+ cells is significantly decreased both in the corpus callosum and in the spinal cord
• at 10 weeks, the % of mt-YFP+ cells in the corpus callosum that are also APC+ is significantly reduced, while the % of APC- Olig2- targeted cells is significantly increased
• surprisingly, the number of mature oligodendrocytes and the size of APC+ cells is increased at 28 weeks of age; enlarged APC+ cells do not co-localize with mt-YFP+ cells but are in fact intensively positive for Olig2 staining
• at 10 weeks of age, non-myelinating Schwann cells in the subcutaneous nerve plexus show a significant decrease of mt-YFP signal
• at 10 weeks of age, tamoxifen-treated mice show clear signs of Schwann cell pathology affecting preferentially small calibre unmyelinated fibers; several Remak bundles appear affected with individual unmyelinated axons touching each other and showing initial signs of axonal degeneration; inner tongue swellings are also observed in myelinated axons
• at 10 weeks of age, tamoxifen-treated mice show a reduction of mt-YFP signal within the sciatic nerve
• tamoxifen-treated mice show death of mature oligodendrocytes followed by compensatory repopulation by untargeted oligodendrocytes
• at 8 weeks of age, several oligodendrocytes undergo dark cell death, a caspase-independent form of death characterized by strong cytoplasmic condensation, chromatin clumping, ruffling of the cell membrane, but no blebbing of the nucleus or plasma membrane
• only a few TUNEL+ apoptotic cells are noted in the corpus callosum at 7 weeks of age
• at 28 weeks of age, non-myelinated large caliber axons and multivesicular disintegration of adaxonal myelin lamellae are observed in the sciatic nerve

cellular
• at 6 weeks of age, oligodendrocytes of tamoxifen-treated mice exhibit swollen mitochondria
• at 8 but not at 6 weeks of age, oligodendrocytes of tamoxifen-treated mice exhibit loss of COX1 staining, indicating impaired mitochondrial function
• cytochrome c is undetectable in several swollen mitochondria in oligodendrocytes at 8 weeks of age

embryo
• at 10 weeks of age, tamoxifen-treated mice show a strong reduction of mt-YFP+ melanoblasts in the outer root sheath of the hair follicle
• at 28 weeks of age, pigmented hair follicles and c-KIT+ melanoblasts are significantly reduced in dorsal skin, suggesting that premature hair greying is caused by progressive loss of melanoblasts that share a common developmental origin with Schwann cells

integument
• at 28 weeks of age, tamoxifen-treated mice show reduced fat deposited in the dermis
• however, general skin structure is normal

pigmentation
• at 28 weeks of age, c-KIT+ melanocytes are significantly reduced in dorsal skin





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last database update
03/14/2017
MGI 6.08
The Jackson Laboratory