All Phenotypes Gt(ROSA)26Sor<tm1Lrsn> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Gt(ROSA)26Sor^tm1Lrsn/Gt(ROSA)26Sor⁺ Prkn^tm1Roo/Prkn^tm1Roo Slc6a3^tm1(cre)Lrsn/Slc6a3⁺ Tfam^tm1Lrsn/Tfam^tm1Lrsn	involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6	MGI:5292517
cn2	Gt(ROSA)26Sor^tm1Lrsn/Gt(ROSA)26Sor⁺ Mfn2^tm1.1Arte/Mfn2^tm1.1Arte Slc6a3^tm1(cre)Lrsn/Slc6a3⁺	involves: 129S1/Sv * 129X1/SvJ	MGI:5440842
cn3	Gt(ROSA)26Sor^tm1Lrsn/Gt(ROSA)26Sor⁺ Slc6a3^tm1(cre)Lrsn/Slc6a3⁺ Tfam^tm1Lrsn/Tfam^tm1Lrsn	involves: 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:5292515
cn4	Afg3l2^tm1Arte/Afg3l2^tm1Arte Gt(ROSA)26Sor^tm1Lrsn/Gt(ROSA)26Sor⁺ Tg(Pcp2-cre)2Mpin/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:5476802
cn5	Afg3l2^tm1Arte/Afg3l2^tm1Arte Gt(ROSA)26Sor^tm1Lrsn/Gt(ROSA)26Sor⁺ Tg(Plp1-cre/ERT)3Pop/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J	MGI:5817781
cn6	Afg3l1^tm1.1Arte/Afg3l1^tm1.1Arte Afg3l2^tm1Arte/Afg3l2^tm1Arte Gt(ROSA)26Sor^tm1Lrsn/Gt(ROSA)26Sor⁺ Tg(Plp1-cre/ERT)3Pop/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * C57BL/6N	MGI:5817784

Allelic Composition	Gt(ROSA)26Sor^tm1Lrsn/Gt(ROSA)26Sor⁺ Prkn^tm1Roo/Prkn^tm1Roo Slc6a3^tm1(cre)Lrsn/Slc6a3⁺ Tfam^tm1Lrsn/Tfam^tm1Lrsn
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)26Sor^tm1Lrsn mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Prkn^tm1Roo mutation (0 available); any Prkn mutation (54 available)
Slc6a3^tm1(cre)Lrsn mutation (1 available); any Slc6a3 mutation (66 available)
Tfam^tm1Lrsn mutation (1 available); any Tfam mutation (14 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

abnormal neuron morphology ( J:176022 )

• 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

loss of dopaminergic neurons ( J:176022 )

abnormal axonal transport ( J:176022 )

• neurons exhibit less intense staining with a retrograde tracer (fluorogold) suggesting impaired retrograde transport and/or uptake of the tracer compared with control cells

Allelic Composition	Gt(ROSA)26Sor^tm1Lrsn/Gt(ROSA)26Sor⁺ Mfn2^tm1.1Arte/Mfn2^tm1.1Arte Slc6a3^tm1(cre)Lrsn/Slc6a3⁺
Genetic Background	involves: 129S1/Sv * 129X1/SvJ

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^tm1Lrsn mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Mfn2^tm1.1Arte mutation (0 available); any Mfn2 mutation (27 available)
Slc6a3^tm1(cre)Lrsn mutation (1 available); any Slc6a3 mutation (66 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

abnormal dorsal striatum morphology ( J:188337 )

• profound reduction in the number of labeled mitochondria in the dorsal striatum

abnormal dopaminergic neuron morphology ( J:188337 )

• mitochondria are spherical and enlarged with disorganized cristae

cellular

abnormal mitochondrial shape ( J:188337 )

• mitochondria in dopaminergic neurons are spherical and enlarged with disorganized cristae

decreased mitochondrial number ( J:188337 )

• profound reduction in the number of labeled mitochondria in the dorsal striatum

increased mitochondrial size ( J:188337 )

• mitochondria in dopaminergic neurons are spherical and enlarged with disorganized cristae

Allelic Composition	Gt(ROSA)26Sor^tm1Lrsn/Gt(ROSA)26Sor⁺ Slc6a3^tm1(cre)Lrsn/Slc6a3⁺ Tfam^tm1Lrsn/Tfam^tm1Lrsn
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^tm1Lrsn mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Slc6a3^tm1(cre)Lrsn mutation (1 available); any Slc6a3 mutation (66 available)
Tfam^tm1Lrsn mutation (1 available); any Tfam mutation (14 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

Mitochondria abnormalities in Tfam^tm1Lrsn/Tfam^tm1Lrsn Slc6a3^tm1(cre)Lrsn/Slc6a3⁺ Gt(ROSA)26Sor^tm1Lrsn/Gt(ROSA)26Sor⁺ neurons

nervous system

abnormal neuron morphology ( J:176022 )

• YFP+ neurons exhibit a progressive reduction in distal axonal mitochondrial numbers compared with control cells

loss of dopaminergic neurons ( J:176022 )

cellular

abnormal mitochondrial physiology ( J:176022 )

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

behavior/neurological

abnormal locomotor behavior ( J:176022 )

• impaired from 20 weeks of age

growth/size/body

weight loss ( J:176022 )

• from 20 weeks of age

muscle

muscle hypertonia ( J:176022 )

• rigidity from 20 weeks of age

Allelic Composition	Afg3l2^tm1Arte/Afg3l2^tm1Arte Gt(ROSA)26Sor^tm1Lrsn/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:
Afg3l2^tm1Arte mutation (0 available); any Afg3l2 mutation (69 available)
Gt(ROSA)26Sor^tm1Lrsn mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Pcp2-cre)2Mpin mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

Abnormal mitochondrial network in Afg3l2^tm1Arte/Afg3l2^tm1Arte Tg(Pcp2-cre)2Mpin/0 Gt(ROSA)26Sor^tm1Lrsn/Gt(ROSA)26Sor⁺ mice

cellular

abnormal Purkinje cell mitochondrial morphology ( J:193564 )

• at 4 weeks, Purkinje cells exhibit fragmentation of mitochondria unlike control cells

• at 6 weeks, mitochondrial fragmentation is very pronounced

nervous system

abnormal Purkinje cell mitochondrial morphology ( J:193564 )

• at 4 weeks, Purkinje cells exhibit fragmentation of mitochondria unlike control cells

• at 6 weeks, mitochondrial fragmentation is very pronounced

abnormal nervous system electrophysiology ( J:193564 )

• Purkinje cell electrophysiological properties are normal at 4 to 5 weeks of age

Allelic Composition	Afg3l2^tm1Arte/Afg3l2^tm1Arte Gt(ROSA)26Sor^tm1Lrsn/Gt(ROSA)26Sor⁺ Tg(Plp1-cre/ERT)3Pop/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

cellular

abnormal mitochondrial shape ( J:237410 )

• at 8 weeks of age, oligodendrocytes in the corpus callosum of tamoxifen-treated mice exhibit fragmented mitochondria, unlike in control mice

dilated mitochondrion ( J:237410 )

• at 8 weeks of age, oligodendrocytes in the corpus callosum of tamoxifen-treated mice exhibit swollen mitochondria, unlike in control mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

abnormal melanoblast morphology ( J:237410 )

• 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

abnormal oligodendrocyte morphology ( J:237410 )

• 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

abnormal Schwann cell morphology ( J:237410 )

• 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

abnormal sciatic nerve morphology ( J:237410 )

• at 10 weeks of age, tamoxifen-treated mice show a reduction of mt-YFP signal within the sciatic nerve

abnormal oligodendrocyte physiology ( J:237410 )

• 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

demyelination ( J:237410 )

• at 28 weeks of age, non-myelinated large caliber axons and multivesicular disintegration of adaxonal myelin lamellae are observed in the sciatic nerve

cellular

dilated mitochondrion ( J:237410 )

• at 6 weeks of age, oligodendrocytes of tamoxifen-treated mice exhibit swollen mitochondria

abnormal mitochondrial physiology ( J:237410 )

• 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

abnormal melanoblast morphology ( J:237410 )

• 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

integument

abnormal dermal layer morphology ( J:237410 )

• however, general skin structure is normal

• at 28 weeks of age, tamoxifen-treated mice show reduced fat deposited in the dermis

pigmentation

decreased melanocyte number ( J:237410 )

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

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