All Phenotypes Tg(Plp1-cre/ERT)3Pop MGI Mouse

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Phenotypes associated with this allele

Allele Symbol
Allele Name
Allele ID

Tg(Plp1-cre/ERT)3Pop
transgene insertion 3, Brian Popko
MGI:2450391

Summary

10 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Rnd2^tm1.1Jya/Rnd2^tm1.1Jya Tg(Plp1-cre/ERT)3Pop/0	B6.Cg-Rnd2^tm1.1Jya Tg(Plp1-cre/ERT)3Pop	MGI:7645369
cn2	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
cn3	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
cn4	Gt(ROSA)26Sor^{tm1(CAG-SNCA)Tanj}/Gt(ROSA)26Sor^{tm1(CAG-SNCA)Tanj} Tg(Plp1-cre/ERT)3Pop/0	involves: 129S6/SvEvTac * C57BL/6J * C57BL/6NCrl * DBA/2	MGI:6473661
cn5	Gt(ROSA)26Sor^tm1(DTA)Jpmb/Gt(ROSA)26Sor⁺ Tg(Plp1-cre/ERT)3Pop/0	involves: 129S/SvEv * C57BL/6 * DBA/2	MGI:5796111
cn6	Cemip^tm1.1Tac/Cemip^tm1.1Tac Tg(Plp1-cre/ERT)3Pop/0	involves: C57BL/6 * C57BL/6NTac * DBA/2	MGI:6117717
cn7	Nfasc^tm1Bhat/Nfasc^tm1Bhat Tg(Plp1-cre/ERT)3Pop/?	involves: C57BL/6 * DBA/2	MGI:3836432
cn8	Afg3l2^tm1Arte/Afg3l2^tm1Arte Tg(Plp1-cre/ERT)3Pop/0	involves: C57BL/6J	MGI:5817780
cn9	Afg3l1^tm1.1Arte/Afg3l1^tm1.1Arte Afg3l2^tm1Arte/Afg3l2^tm1Arte Tg(Plp1-cre/ERT)3Pop/0	involves: C57BL/6J * C57BL/6N	MGI:5817783
tg10	Tg(Plp1-cre/ERT)3Pop/0	involves: C57BL/6 * DBA/2	MGI:3696409

Allelic Composition	Rnd2^tm1.1Jya/Rnd2^tm1.1Jya Tg(Plp1-cre/ERT)3Pop/0
Genetic Background	B6.Cg-Rnd2^tm1.1Jya Tg(Plp1-cre/ERT)3Pop

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rnd2^tm1.1Jya mutation (0 available); any Rnd2 mutation (53 available)
Tg(Plp1-cre/ERT)3Pop mutation (2 available)

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

nervous system

decreased myelin sheath thickness ( J:309719 )

• mice show decreased myelin thickness in the corpus callosum 2 weeks after tamoxifen administration, with increased average g-ratios

increased myelin sheath thickness ( J:309719 )

• mice show increased myelin thickness 4 weeks after tamoxifen administration, with decreased average g-ratios

abnormal myelination ( J:309719 )

• mice show decreased myelin thickness in the corpus callosum two weeks after tamoxifen administration and increased myelin thickness four weeks after tamoxifen administration

• mice treated with tamoxifen for 5 days at 8-9 weeks of age show decreased MBP staining in the brain and decreased expression levels of MBP and CNPase two weeks after tamoxifen administration and increased MBP staining in the brain and increased expression levels of MBP and CNPase four weeks after tamoxifen administration

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

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(Plp1-cre/ERT)3Pop mutation (2 available)

♀	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

Allelic Composition	Afg3l1^tm1.1Arte/Afg3l1^tm1.1Arte 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 * C57BL/6N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Afg3l1^tm1.1Arte mutation (0 available); any Afg3l1 mutation (35 available)
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(Plp1-cre/ERT)3Pop mutation (2 available)

♀	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

Allelic Composition	Gt(ROSA)26Sor^{tm1(CAG-SNCA)Tanj}/Gt(ROSA)26Sor^{tm1(CAG-SNCA)Tanj} Tg(Plp1-cre/ERT)3Pop/0
Genetic Background	involves: 129S6/SvEvTac * C57BL/6J * C57BL/6NCrl * DBA/2

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^{tm1(CAG-SNCA)Tanj} mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Plp1-cre/ERT)3Pop mutation (2 available)

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

mortality/aging

premature death ( J:283567 )

• approximately 30% of males exhibit sudden death 20 weeks after tamoxifen treatment

behavior/neurological

impaired coordination ( J:283567 )

• mice show deficits in motor coordination and balance on the rotarod at 20 to 50 weeks after tamoxifen induction

• however, tamoxifen induced mice show no differences in immobility in the forced swim test from controls

decreased locomotor activity ( J:283567 )

• 20 to 50 weeks after tamoxifen induction, mice show deterioration of performance in the open field, having shorter moving distance

• however, tamoxifen treated mice do not show muscle abnormalities and no differences in grip handling

nervous system

nervous system phenotype ( J:283567 )

N	• tamoxifen treated mice do not show neuronal loss in the anterior horn, the cerebellum, brainstem, substantia nigra and striatum

abnormal glial cell morphology ( J:283567 )

• ubiquitin accumulation is seen in glial cells after tamoxifen induction

• tamoxifen-treated mice show increased GFAP+ astrocytes and Iba1+ microglial cells in the brain stem indicating accelerated inflammatory response with age

abnormal neuron morphology ( J:283567 )

• ubiquitin accumulation is seen in neurons after tamoxifen induction

alpha-synuclein inclusion body ( J:283567 )

• tamoxifen treated mice show alpha-synuclein inclusions mainly aggregated in oligodendrocytes

• perinuclear alpha-synuclein inclusions are seen in certain neurons, especially those located in the brainstem and putamen, 1 week after tamoxifen induction

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
multiple system atrophy		DOID:4752		J:283567

Allelic Composition	Gt(ROSA)26Sor^tm1(DTA)Jpmb/Gt(ROSA)26Sor⁺ Tg(Plp1-cre/ERT)3Pop/0
Genetic Background	involves: 129S/SvEv * C57BL/6 * DBA/2

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^tm1(DTA)Jpmb mutation (2 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Plp1-cre/ERT)3Pop mutation (2 available)

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

mortality/aging

premature death ( J:234435 )

• about 50% of mice die 52 weeks after tamoxifen injection

nervous system

seizures ( J:234435 )

• mice exhibit seizures starting around 40 weeks after tamoxifen injection

CNS inflammation ( J:234435 )

• focal lesions in tamoxifen treated mice are sites of active inflammation, frequently infiltrated by T cells, and contain a high density of microglia or macrophages

• mice show increased CD3+ T cells in the CNS as early as 7 weeks after tamoxifen injection, increased numbers of CD4+ T cells in the CNS at 10 and 40 weeks after tamoxifen injection, and increased numbers of MHCII+B7+ (CD80+CD86+) dendritic cells at 40 weeks after tamoxifen injection

abnormal nervous system morphology ( J:234435 )

• all recovered tamoxifen-treated mice develop secondary, late-onset neurological symptoms and demyelinating disease starting around 40 weeks after injection

• mice injected with MOG(35-55)-coupled polylactic-co-glycolic acid nanoparticles 32 weeks after tamoxifen injection show inhibition of disease progression

• mice exhibit rare focal lesions in the brainstem, cerebellum, and spinal cord at 40 weeks after tamoxifen injection

• at 1 year after tamoxifen injection, focal lesions in these regions are no longer seen

abnormal brain white matter morphology ( J:234435 )

• white matter lesions in tamoxifen injected mice show presence of macrophages containing myelin debris and unmyelinated axons, indicating ongoing demyelination

decreased oligodendrocyte number ( J:234435 )

• tamoxifen treated mice exhibit loss of oligodendrocytes, peaking 5 weeks after injection and recovering by 10 weeks

• brainstem shows an approximate 50% decrease in oligodendrocytes at 1 year after tamoxifen treatment

• however, substantial oligodendrocyte loss in other CNS areas is not seen at 1 year after tamoxifen treatment

decreased myelin sheath thickness ( J:234435 )

• thinner myelin in both tamoxifen treated and untreated mice (due to leakiness of the cre-expressing transgene)

axon degeneration ( J:234435 )

• axonal loss in the ventrolateral white matter of the cervical spinal cord (40%) and the optic nerve (55%) at 1 year after tamoxifen treatment

demyelination ( J:234435 )

• tamoxifen treated mice exhibit widespread CNS demyelination, peaking 5 weeks after injection and recovering by 10 weeks

• mice exhibit widespread myelin loss at 1 year after tamoxifen injection

• mice not treated with tamoxifen show some myelin loss in most CNS areas at 52 weeks of age, indicating leakiness of the cre-expressing transgene

• untreated mice exhibit about 30% fewer unmyelinated axons in the corpus callosum compared to tamoxifen treated mice

behavior/neurological

abnormal motor coordination/balance ( J:234435 )

• mice show impaired motor skills starting around 40 weeks after tamoxifen injection

ataxia ( J:234435 )

• tamoxifen treated mice exhibit severe ataxia starting around 40 weeks after injection

seizures ( J:234435 )

• mice exhibit seizures starting around 40 weeks after tamoxifen injection

growth/size/body

weight loss ( J:234435 )

• mice show weight loss starting around 40 weeks after tamoxifen injection

hematopoietic system

increased activated T cell number ( J:234435 )

• activated CD4+ T cells are present in the CNS at 10 weeks after tamoxifen injection and both activated CD4+ T cells and antigen-presenting dendritic cells are present in the CNS 40 week after tamoxifen injection

immune system

increased activated T cell number ( J:234435 )

lymph node inflammation ( J:234435 )

• total numbers of CD4+ T cells, CD8+ T cells, B cells, monocytes, and dendritic cells in the CNS-draining cervical lymph nodes of tamoxifen treated mice is higher than in controls

autoimmune response ( J:234435 )

• at 40 weeks after tamoxifen injection, autoreactive T cells capable of proliferating in response to stimulation with recombinant MOG protein are seen in the spleen and cervical lymph nodes indicating an adaptive autoimmune response against myelin

CNS inflammation ( J:234435 )

• focal lesions in tamoxifen treated mice are sites of active inflammation, frequently infiltrated by T cells, and contain a high density of microglia or macrophages

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
multiple sclerosis		DOID:2377	OMIM:612594 OMIM:612595 OMIM:612596	J:234435

Allelic Composition	Cemip^tm1.1Tac/Cemip^tm1.1Tac Tg(Plp1-cre/ERT)3Pop/0
Genetic Background	involves: C57BL/6 * C57BL/6NTac * DBA/2

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cemip^tm1.1Tac mutation (0 available); any Cemip mutation (67 available)
Tg(Plp1-cre/ERT)3Pop mutation (2 available)

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

nervous system

abnormal Schwann cell physiology ( J:244311 )

• tamoxifen-treated myelinated Schwann cells in culture exhibit reduced dedifferentiation compared with wild-type cells

Allelic Composition	Nfasc^tm1Bhat/Nfasc^tm1Bhat Tg(Plp1-cre/ERT)3Pop/?
Genetic Background	involves: C57BL/6 * DBA/2

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nfasc^tm1Bhat mutation (0 available); any Nfasc mutation (61 available)
Tg(Plp1-cre/ERT)3Pop mutation (2 available)

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

nervous system

abnormal axon morphology ( J:145846 )

• after 20 days of tamoxifen treatment

• septal morphology of axons becomes progressively disorganized

• axolemma becomes detached from myelin loops

decreased nerve conduction velocity ( J:145846 )

• moderate reduction of tibial/plantar conduction velocity in mice injected at days 23-33 with tamoxifen measured around 86 days of age

Allelic Composition	Afg3l2^tm1Arte/Afg3l2^tm1Arte Tg(Plp1-cre/ERT)3Pop/0
Genetic Background	involves: C57BL/6J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Afg3l2^tm1Arte mutation (0 available); any Afg3l2 mutation (69 available)
Tg(Plp1-cre/ERT)3Pop mutation (2 available)

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

behavior/neurological

impaired coordination ( J:237410 )

• at 90 weeks of age, tamoxifen-treated mice show a mild but significant impairment in motor performance on an accelerating rotarod test

• however, no abnormalities in cage behavior are observed

nervous system

abnormal oligodendrocyte morphology ( J:237410 )

• at 90 weeks of age, tamoxifen-treated mice show only a few bigger oligodendrocytes (APC+ cells) in the corpus callosum

• by 86 weeks of age, oligodendrocytes in the spinal cord white matter contain enlarged mitochondria with disrupted cristae

decreased myelin sheath thickness ( J:237410 )

• at 56 weeks of age, a few axons in the spinal cord white matter exhibit thin myelin

increased myelin sheath thickness ( J:237410 )

• at 90 weeks of age, tamoxifen-treated mice show thickened myelin in the antero-lateral funiculi spinal cord white matter

abnormal spinal cord white matter morphology ( J:237410 )

• at 56 weeks of age, a few axons in the spinal cord white matter exhibit thin myelin while others show adaxonal myelin detachment and vacuolization

• by 86 weeks, degenerating axons are surrounded by damaged myelin or contain accumulation of material

axon degeneration ( J:237410 )

• at 90 weeks of age, tamoxifen-treated mice show abnormal myelin profiles characterized by myelin thickening, infoldings and myelin whorls, indicative of axonal degeneration, in the spinal cord

• however, myelination and axonal integrity is largely normal at 56 weeks of age

dysmyelination ( J:237410 )

• at 56 weeks, and more prominently at 86 weeks of age, tamoxifen-treated mice exhibit myelin disruption and myelin detachment in the spinal cord white matter

• however, no obvious demyelination is detected up to 90 weeks of age

cellular

abnormal mitochondrial crista morphology ( J:237410 )

• by 86 weeks of age, oligodendrocytes in the spinal cord white matter exhibit disrupted mitochondrial cristae

increased mitochondrial size ( J:237410 )

• by 86 weeks of age, oligodendrocytes in the spinal cord white matter contain enlarged mitochondria

growth/size/body

growth/size/body region phenotype ( J:237410 )

N	• tamoxifen-treated mice show no significant weight loss up 90 weeks of age

Allelic Composition	Afg3l1^tm1.1Arte/Afg3l1^tm1.1Arte Afg3l2^tm1Arte/Afg3l2^tm1Arte Tg(Plp1-cre/ERT)3Pop/0
Genetic Background	involves: C57BL/6J * C57BL/6N

Find Mice

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

growth/size/body

decreased body fat mass ( J:237410 )

• at 13 and 28 weeks of age, tamoxifen-treated mice exhibit significantly decreased fat mass relative to single Afg3l1^tm1.1Arte homozygous (control) mice

decreased body weight ( J:237410 )

• starting at 8 weeks of age, tamoxifen-treated mice show decreased body weight relative to control mice

• difference in body weight persists even after adding food pellets directly in the cage

behavior/neurological

impaired coordination ( J:237410 )

• at 11-13 weeks of age, tamoxifen-treated mice spend less time on the rotating rod than control mice

• during a beam walking test, the number of foot slips is significantly higher at 13 weeks and dramatically increased at 28 weeks of age relative to that in control mice

nervous system

microgliosis ( J:237410 )

• demyelination is associated with microglia activation

• tamoxifen-treated mice exhibit activated microglia in the corpus callosum at 28 weeks of age

abnormal brain white matter morphology ( J:237410 )

• tamoxifen-treated mice show marked loss of white matter in the corpus callosum, internal capsule, and cerebellum at 28 weeks of age

astrocytosis ( J:237410 )

• demyelination is associated with astrocyte activation, as shown by upregulation of GFAP in spinal cord and brain lysates at 10 and 28 weeks of age

abnormal spinal cord white matter morphology ( J:237410 )

• tamoxifen-treated mice show progressive demyelination in the spinal cord white matter, with some axons showing adaxonal myelin detachment at 13 weeks and marked signs of demyelination at 18 weeks of age

• the g ratio, expressing the ratio between the diameter of the inner axon and the total fiber diameter, is significantly increased at 28 weeks of age

axon degeneration ( J:237410 )

• tamoxifen-treated mice show signs of secondary axonal degeneration in the spinal cord, with accumulation of organelles and material in axons at 28 weeks of age

demyelination ( J:237410 )

• tamoxifen-treated mice show progressive demyelination in the lumbar spinal cord, resulting in demyelinated and degenerating axons as well as dark cells in the antero-lateral funiculus at 28 weeks of age

• Gallyas' silver staining of brain myelinated tracts showed prominent loss of white matter in the corpus callosum, internal capsule, and cerebellum at 28 weeks of age

• progressive loss of myelin is confirmed by western blot analysis of myelin proteins in spinal cord and brain lysates at 10 and 28 weeks of age

pigmentation

abnormal coat/hair pigmentation ( J:237410 )

• tamoxifen-treated mice show premature and progressive hair greying starting ventrally close to the forelimbs at 10 weeks, resulting in a grey belly at 17 weeks, and finally extending to the dorsal skin at 28 weeks of age; no such phenotype is observed in control mice

adipose tissue

decreased body fat mass ( J:237410 )

• at 13 and 28 weeks of age, tamoxifen-treated mice exhibit significantly decreased fat mass relative to single Afg3l1^tm1.1Arte homozygous (control) mice

hematopoietic system

microgliosis ( J:237410 )

• demyelination is associated with microglia activation

• tamoxifen-treated mice exhibit activated microglia in the corpus callosum at 28 weeks of age

immune system

microgliosis ( J:237410 )

• demyelination is associated with microglia activation

• tamoxifen-treated mice exhibit activated microglia in the corpus callosum at 28 weeks of age

integument

abnormal coat/hair pigmentation ( J:237410 )

Allelic Composition	Tg(Plp1-cre/ERT)3Pop/0
Genetic Background	involves: C57BL/6 * DBA/2

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Plp1-cre/ERT)3Pop mutation (2 available)

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

normal phenotype

no abnormal phenotype detected ( J:81627 )

• mice ae fertile and appear normal; expression of cre is primarily restricted to myelinating oligodendrocytes of the CNS

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