Phenotypes associated with this allele

• Allele Symbol: Gt(ROSA)26Sor^tm1(DTA)Mrc
• Allele Name: targeted mutation 1, Mario R Capecchi
• Allele ID: MGI:3618991
• Summary: 10 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Gt(ROSA)26Sor^tm1(DTA)Mrc/Gt(ROSA)26Sor^+ Olig1^tm1(cre)Rth/Olig1^+	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ	MGI:3620048
cn2	Pax7^tm1(cre/ERT2)Gaka/Pax7^+ Gt(ROSA)26Sor^tm1(DTA)Mrc/Gt(ROSA)26Sor^+	involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6	MGI:5141594
cn3	Gt(ROSA)26Sor^tm1(DTA)Mrc/Gt(ROSA)26Sor^+ Myf5^tm1(cre)Mrc/Myf5^+	involves: 129S1/Sv * 129X1/SvJ	MGI:3783871
cn4	Gt(ROSA)26Sor^tm1(DTA)Mrc/Gt(ROSA)26Sor^+ Myf6^tm1(cre)Mrc/Myf6^+	involves: 129S1/Sv * 129X1/SvJ	MGI:3783879
cn5	Bmi1^tm1(cre/ERT)Mrc/Bmi1^+ Gt(ROSA)26Sor^tm1(DTA)Mrc/Gt(ROSA)26Sor^+	involves: 129S1/Sv * 129X1/SvJ	MGI:3805820
cn6	Gt(ROSA)26Sor^tm1(DTA)Mrc/Gt(ROSA)26Sor^+ Myf5^tm1.1(cre)Mrc/Myf5^+	involves: 129S1/Sv * 129X1/SvJ	MGI:3783863
cn7	Tcf7l2^tm3.1(cre/ERT2)Mrc/Tcf7l2^+ Gt(ROSA)26Sor^tm1(DTA)Mrc/Gt(ROSA)26Sor^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:5141595
cn8	Gt(ROSA)26Sor^tm1(DTA)Mrc/Gt(ROSA)26Sor^+ Chrna7^tm2.1(cre)Swr/Chrna7^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:5662242
cn9	Gt(ROSA)26Sor^tm1(DTA)Mrc/Gt(ROSA)26Sor^tm1(DTA)Mrc Myf5^tm1(cre)Mrc/Myf5^tm1(cre)Mrc	involves: 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:3710995
cn10	Gt(ROSA)26Sor^tm1(DTA)Mrc/? Tg(Rlbp1-cre/ERT2,-EGFP)1Wshn/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * CBA	MGI:5491505

Genotype
MGI:3620048

cn1

• Allelic Composition: Gt(ROSA)26Sor^tm1(DTA)Mrc/Gt(ROSA)26Sor⁺; Olig1^tm1(cre)Rth/Olig1⁺
• Genetic Background: involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ

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

mortality/aging

lethality throughout fetal growth and development, complete penetrance ( J:105927 )

• double heterozygotes are viable to E18.0 but no live mice are recovered

nervous system

absent oligodendrocytes ( J:105927 )

• oligodendrocytes cannot be detected in mutant embryos examined from E12.5-18

decreased motor neuron number ( J:105927 )

• at E10.0, few motor neurons are detectable in the ventral spinal cord compared to wild-type; this result is consistent from E10.5-14

Genotype
MGI:5141594

cn2

• Allelic Composition: Pax7^{tm1(cre/ERT2)Gaka}/Pax7⁺; Gt(ROSA)26Sor^tm1(DTA)Mrc/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6

muscle

decreased satellite cell number ( J:174914 )

• 83-84% of satellite cells are ablated in the right tibialis anterior muscle after 5 doses of tamoxifen and 5days after muscle damage induced by BaCl2 injection

skeletal muscle fibrosis ( J:174914 )

• reduced fibroblast expansion by 52% 5 days after muscle injury in tamoxifen treated mice

impaired skeletal muscle regeneration ( J:174914 )

• 89% reduction in regenerating myofibers 5 days after muscle injury in tamoxifen treated mice

• muscle regeneration dramatically impaired 28 days after injury

• right tibialis anterior muscle entirely fibrotic at 28 days and uninjured left tibialis anterior is reduced by 38%

• similar result when damage induced with cardiotoxin, no recovery after 56 days

Genotype
MGI:3783871

cn3

• Allelic Composition: Gt(ROSA)26Sor^tm1(DTA)Mrc/Gt(ROSA)26Sor⁺; Myf5^tm1(cre)Mrc/Myf5⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ

mortality/aging

mortality/aging ( J:133338 )

N • 90% of pups are viable with a normal life span and normal musculature

skeleton

asymmetric sternocostal joints ( J:133338 )

• occasionally

abnormal rib morphology ( J:133338 )

• reduced costochondral and costosternal regions of ribs

• newborns with normal rib cages but occasional anomalies

• floating ribs occasionally misshapen

• occasional osseous knob-like protrusions

rib fusion ( J:133338 )

• occasional fusion of cartillagenous portions of ribs

Genotype
MGI:3783879

cn4

• Allelic Composition: Gt(ROSA)26Sor^tm1(DTA)Mrc/Gt(ROSA)26Sor⁺; Myf6^tm1(cre)Mrc/Myf6⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ

mortality/aging

neonatal lethality, complete penetrance ( J:133338 )

• pups are immobile and die shortly after birth

muscle

abnormal myogenesis ( J:133338 )

• myogenesis appears normal at E12.5

• increasing apoptosis until all differentiating myofibers are either dead or dying at E18.5

abnormal skeletal muscle fiber morphology ( J:133338 )

• newborns lack differentiated myofibers

• basophilic clumps of cellular debris suggest skeletal muscle forms and then degenerates

Genotype
MGI:3805820

cn5

• Allelic Composition: Bmi1^{tm1(cre/ERT)Mrc}/Bmi1⁺; Gt(ROSA)26Sor^tm1(DTA)Mrc/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ

mortality/aging

premature death ( J:138364 )

• mice die 2 to 3 days following administration of tamoxifen for three consecutive days after weaning

digestive/alimentary system

abnormal duodenum crypts of Lieberkuhn morphology ( J:138364 )

• following administration of one dose of tamoxifen after weaning, mice exhibit areas of the duodenum that are devoid of crypt cells

• however, crypt cells recover by 9 months of age

abnormal jejunum crypts of Lieberkuhn morphology ( J:138364 )

• following administration of one dose of tamoxifen after weaning, mice exhibit areas of the jejunum that are devoid of crypt cells

• however, crypt cells recover by 9 months of age

growth/size/body

slow postnatal weight gain ( J:138364 )

• following administration of one dose of tamoxifen after weaning

• however, normal weight is recovered by 9 months of age

endocrine/exocrine glands

abnormal duodenum crypts of Lieberkuhn morphology ( J:138364 )

• following administration of one dose of tamoxifen after weaning, mice exhibit areas of the duodenum that are devoid of crypt cells

• however, crypt cells recover by 9 months of age

abnormal jejunum crypts of Lieberkuhn morphology ( J:138364 )

• following administration of one dose of tamoxifen after weaning, mice exhibit areas of the jejunum that are devoid of crypt cells

• however, crypt cells recover by 9 months of age

Genotype
MGI:3783863

cn6

• Allelic Composition: Gt(ROSA)26Sor^tm1(DTA)Mrc/Gt(ROSA)26Sor⁺; Myf5^{tm1.1(cre)Mrc}/Myf5⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ

mortality/aging

neonatal lethality, complete penetrance ( J:133338 )

• pups fail to survive after birth

muscle

muscle phenotype ( J:133338 )

N • normal myogenesis

N • both fast and slow fibers with normal morphology

N • functional and utrastructural integrity normal

skeleton

abnormal rib morphology ( J:133338 )

• newborns with severely deformed ribs

Genotype
MGI:5141595

cn7

• Allelic Composition: Tcf7l2^{tm3.1(cre/ERT2)Mrc}/Tcf7l2⁺; Gt(ROSA)26Sor^tm1(DTA)Mrc/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6

muscle

abnormal muscle morphology ( J:174914 )

• 42% reduction in muscle connective tissue fibroblasts after 5 doses of tamoxifen

decreased satellite cell number ( J:174914 )

• ablation of fibroblasts leads to 51% reduction in muscle satellite cells 5 days post injury

abnormal muscle regeneration ( J:174914 )

• at 3 days post injury fibroblasts are reduced 19% but myofiber regeneration is increased 5 fold

• leads to depletion of satellite cell pool and reduction in regenerating myofibers at 5 days

• tibialis anterior muscle is regenerated at 28 days after injury but somewhat smaller in cross-sectional area

• satellite cell numbers have recovered after 28 days

• smaller diameter of regenerated myofibers

• muscle size differences are no longer significant at 56 days after injury

Genotype
MGI:5662242

cn8

• Allelic Composition: Gt(ROSA)26Sor^tm1(DTA)Mrc/Gt(ROSA)26Sor⁺; Chrna7^{tm2.1(cre)Swr}/Chrna7⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6

mortality/aging

perinatal lethality, complete penetrance ( J:223063 )

• mice are stillborn

embryo

embryo phenotype ( J:223063 )

N • placenta organization is grossly normal

abnormal rostral-caudal axis patterning ( J:223063 )

• exaggerated curvature

• however, supplementation with choline improves caudal body axis size

delayed caudal neuropore closure ( J:223063 )

spina bifida ( J:223063 )

• visible as early as E11.5

• evident at E16.5 without full penetrance

• open spina bifida in 9 of 13 pups

• treatment with oral nicotine increases spina bifida incidence and severity

• however, supplementation with folic acid and choline reduces frequency of occurrence

craniofacial

abnormal craniofacial morphology ( J:223063 )

• rare and restricted to the mandible

macrodontia ( J:223063 )

• enlarged teeth at E16.5

short mandible ( J:223063 )

flat head ( J:223063 )

• in stillborn mice

growth/size/body

macrodontia ( J:223063 )

• enlarged teeth at E16.5

flat head ( J:223063 )

• in stillborn mice

enlarged pancreas ( J:223063 )

abnormal abdominal wall morphology ( J:223063 )

• with peritoneal membrane enclosing the extruded liver and intestine at E16.5

omphalocele ( J:223063 )

• evident at E16.5 without full penetrance

• protrusion of abdominal organs (liver and intestines) suggestive of an omphalocele

enlarged liver ( J:223063 )

• at E16.5

limbs/digits/tail

abnormal limb bone morphology ( J:223063 )

• abnormal proportioned limbs in stillborn mice

abnormal tail morphology ( J:223063 )

• reminiscent of Grhl3^ct

• reverted tail tip

• tail defects are not improved by folic acid supplementation

• however, supplementation with choline improves tail bud defects

nervous system

delayed caudal neuropore closure ( J:223063 )

spina bifida ( J:223063 )

• visible as early as E11.5

• evident at E16.5 without full penetrance

• open spina bifida in 9 of 13 pups

• treatment with oral nicotine increases spina bifida incidence and severity

• however, supplementation with folic acid and choline reduces frequency of occurrence

abnormal dorsal root ganglion morphology ( J:223063 )

• extruded dorsal root ganglia at E16.5

dorsal root ganglion hypoplasia ( J:223063 )

vision/eye

abnormal retina pigment epithelium morphology ( J:223063 )

• absence or disorganized at E16.5

behavior/neurological

hunched posture ( J:223063 )

• in stillborn mice

digestive/alimentary system

enlarged salivary gland ( J:223063 )

• at E16.5

endocrine/exocrine glands

enlarged salivary gland ( J:223063 )

• at E16.5

enlarged pancreas ( J:223063 )

hematopoietic system

anemia ( J:223063 )

• in some embryos

liver/biliary system

enlarged liver ( J:223063 )

• at E16.5

pigmentation

abnormal retina pigment epithelium morphology ( J:223063 )

• absence or disorganized at E16.5

skeleton

macrodontia ( J:223063 )

• enlarged teeth at E16.5

short mandible ( J:223063 )

abnormal limb bone morphology ( J:223063 )

• abnormal proportioned limbs in stillborn mice

Genotype
MGI:3710995

cn9

• Allelic Composition: Gt(ROSA)26Sor^tm1(DTA)Mrc/Gt(ROSA)26Sor^tm1(DTA)Mrc; Myf5^tm1(cre)Mrc/Myf5^tm1(cre)Mrc
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6

growth/size/body

decreased body size ( J:120967 )

• 8% to 10% of mice are born small and perform poorly

behavior/neurological

weakness ( J:120967 )

• mice are normal at birth but gradually develop weakness and reduced vitality leasing to their death

Genotype
MGI:5491505

cn10

• Allelic Composition: Gt(ROSA)26Sor^tm1(DTA)Mrc/?; Tg(Rlbp1-cre/ERT2,-EGFP)1Wshn/0
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * CBA

vision/eye

abnormal blood-retina barrier function ( J:192243 )

• Muller cell loss results in breakdown of the blood-retinal barrier 1-2 weeks after tamoxifen treatment; intense areas of focal vascular leak develop after 2 months, and persisting for at least 5 months

• retinal vascular permeability increases by 125% relative to controls after 2 doses of tamoxifen, and by 189% after 5 doses

abnormal retina morphology ( J:192243 )

• after tamoxifen administration, Muller cell loss is detected within 1 day; retinopathy develops subsequently

• 2 weeks after tamoxifen treatment, protrusion of photoreceptor cell bodies into the subretinal space is observed in areas of Muller cell loss

abnormal retina vasculature morphology ( J:192243 )

• 7 days after tamoxifen treatment, tortuous retinal vessels are observed at all three levels of the retinal vascular network

abnormal retina blood vessel morphology ( J:192243 )

• vascular telangiectasis develops by 7 days after treatment, and vascular tufts are observed from 2 months after treatment

retina neovascularization ( J:192243 )

• 2 months following tamoxifen treatment, abnormal vessels appear in the deep retina; new vessels originate from the inner retina

abnormal Muller cell morphology ( J:192243 )

• after tamoxifen administration, Muller cell loss is detected within 1 day

abnormal retina cone cell outer segment morphology ( J:192243 )

• patchy loss of cone photoreceptor outer segments is after tamoxifen treatment; this proceeds for 14 days, then stabilizes 28 days after tamoxifen induction

disorganized photoreceptor outer segment ( J:192243 )

• in areas of Muller cell loss 2 weeks after tamoxifen treatment

abnormal retina pigment epithelium morphology ( J:192243 )

• in regions of neovascularization, RPE clumping, proliferation and migration into regions of the new vessels are observed

abnormal retina inner limiting membrane morphology ( J:192243 )

• 2 weeks after tamoxifen treatment, loss of the electron-dense end feet of Muller cells occurs, with loss of Muller cell bodies

abnormal retina outer limiting membrane morphology ( J:192243 )

• appears disorganized in areas of Muller cell loss 2 weeks after tamoxifen treatment

abnormal eye electrophysiology ( J:192243 )

• 6 weeks after tamoxifen treatment, a- and b-wave responses are significantly reduced compared to controls; both rod- and cone-derived b-waves are affected

abnormal cone electrophysiology ( J:192243 )

abnormal rod electrophysiology ( J:192243 )

• in areas of Muller cell loss 2 weeks after tamoxifen treatment

nervous system

abnormal Muller cell morphology ( J:192243 )

• after tamoxifen administration, Muller cell loss is detected within 1 day

abnormal retina cone cell outer segment morphology ( J:192243 )

• patchy loss of cone photoreceptor outer segments is after tamoxifen treatment; this proceeds for 14 days, then stabilizes 28 days after tamoxifen induction

disorganized photoreceptor outer segment ( J:192243 )

• in areas of Muller cell loss 2 weeks after tamoxifen treatment

abnormal blood-retina barrier function ( J:192243 )

• Muller cell loss results in breakdown of the blood-retinal barrier 1-2 weeks after tamoxifen treatment; intense areas of focal vascular leak develop after 2 months, and persisting for at least 5 months

• retinal vascular permeability increases by 125% relative to controls after 2 doses of tamoxifen, and by 189% after 5 doses

cardiovascular system

abnormal retina vasculature morphology ( J:192243 )

• 7 days after tamoxifen treatment, tortuous retinal vessels are observed at all three levels of the retinal vascular network

abnormal retina blood vessel morphology ( J:192243 )

• vascular telangiectasis develops by 7 days after treatment, and vascular tufts are observed from 2 months after treatment

retina neovascularization ( J:192243 )

• 2 months following tamoxifen treatment, abnormal vessels appear in the deep retina; new vessels originate from the inner retina

pigmentation

abnormal retina pigment epithelium morphology ( J:192243 )

• in regions of neovascularization, RPE clumping, proliferation and migration into regions of the new vessels are observed