Phenotypes associated with this allele

• Allele Symbol: Tg(Postn-cre)1Sjc
• Allele Name: transgene insertion 1, Simon J Conway
• Allele ID: MGI:3775923
• Summary: 3 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Nf2^tm2Gth/Nf2^tm2Gth Tg(Postn-cre)1Sjc/0	involves: 129P2/OlaHsd * FVB/NTac	MGI:5619302
cn2	Nf1^tm1Par/Nf1^tm1Tyj Tg(Postn-cre)1Sjc/0	involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ	MGI:3776057
cn3	Klf5^tm2.1Rng/Klf5^tm2.1Rng Tg(Postn-cre)1Sjc/0	involves: C57BL/6	MGI:4421819

Genotype
MGI:5619302

cn1

• Allelic Composition: Nf2^tm2Gth/Nf2^tm2Gth; Tg(Postn-cre)1Sjc/0
• Genetic Background: involves: 129P2/OlaHsd * FVB/NTac

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

mortality/aging

premature death ( J:216420 )

• mice show reduced life span

behavior/neurological

impaired righting response ( J:216420 )

• mice exhibit difficulty in righting themselves

impaired swimming ( J:216420 )

trunk curl ( J:216420 )

• in the trunk curl test, mice do not reach for the horizontal platform when suspended by the tail and tend to curl in toward their abdomen

head bobbing ( J:216420 )

head tilt ( J:216420 )

head tossing ( J:216420 )

circling ( J:216420 )

hearing/vestibular/ear

abnormal auditory brainstem response waveform shape ( J:216420 )

• ABR waveform analysis indicates a reduction in the first ABR wave amplitude at 6 and 8 months of age and a reduction in summating potential amplitude at 10 months of age, indicating a functional disruption in the cochlear synapse and/or cochlear nerve

increased or absent threshold for auditory brainstem response ( J:216420 )

• mice exhibit a progressive increase in ABR threshold

sensorineural hearing loss ( J:216420 )

• sensorineural hearing loss that is temporally correlated with tumorigenesis

nervous system

increased neurofibrosarcoma incidence ( J:216420 )

• most mice show only multiple large schwannomas, but 5 of 16 mice show tumor lesions consistent with malignant peripheral nerve sheath tumors

increased Schwannoma incidence ( J:216420 )

• mice develop slow-growing, low-grade schwannomas that are seen by 5 months of age

• schwannomas are seen in the dorsal root ganglion and proximal spine nerve by 8 months, and in peripheral, cranial, and spinal nerves (such as of the trigeminal and facial nerves) by 10 months

• aberrant Schwann cell growth is seen in cranial nerve VIII proximal to its entry into the inner ear, including tumors in Scarpas ganglion

• all mice exhibit vestibular schwannomas

increased Schwann cell number ( J:216420 )

• Schwann cell hyperplasia in the spinal ganglion

enlarged dorsal root ganglion ( J:216420 )

• by 5 months of age, all mice show enlargement of the dorsal root ganglion

abnormal spinal nerve morphology ( J:216420 )

• by 5 months of age, all mice show enlargement of the proximal spinal nerve roots

neoplasm

increased neurofibrosarcoma incidence ( J:216420 )

• most mice show only multiple large schwannomas, but 5 of 16 mice show tumor lesions consistent with malignant peripheral nerve sheath tumors

increased Schwannoma incidence ( J:216420 )

• mice develop slow-growing, low-grade schwannomas that are seen by 5 months of age

• schwannomas are seen in the dorsal root ganglion and proximal spine nerve by 8 months, and in peripheral, cranial, and spinal nerves (such as of the trigeminal and facial nerves) by 10 months

• aberrant Schwann cell growth is seen in cranial nerve VIII proximal to its entry into the inner ear, including tumors in Scarpas ganglion

• all mice exhibit vestibular schwannomas

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
vestibular schwannomatosis		DOID:0111252	OMIM:101000	J:216420

Genotype
MGI:3776057

cn2

• Allelic Composition: Nf1^tm1Par/Nf1^tm1Tyj; Tg(Postn-cre)1Sjc/0
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ

mortality/aging

premature death ( J:131914 )

• only 6 of 32 mice survived beyond 4 weeks of age

neoplasm

neoplasm ( J:131914 )

N • unlike mice crossed to Tg(P0-Cre)1Gth tumors are not seen in surviving adults

embryo

abnormal neural crest cell morphology ( J:131914 )

• increase in the frequency of neural crest stem cells in the sympathetic chain and sciatic nerve, but not the gut, at E15 but not in surviving adults

nervous system

abnormal neural crest cell morphology ( J:131914 )

• increase in the frequency of neural crest stem cells in the sympathetic chain and sciatic nerve, but not the gut, at E15 but not in surviving adults

Genotype
MGI:4421819

cn3

• Allelic Composition: Klf5^tm2.1Rng/Klf5^tm2.1Rng; Tg(Postn-cre)1Sjc/0
• Genetic Background: involves: C57BL/6

Fibroblast-specific deletion of Klf5 attenuates cardiac hypertrophy and fibrosis after TAC in Klf5^tm2.1Rng/Klf5^tm2.1Rng Tg(Postn-cre)1Sjc mice

mortality/aging

increased susceptibility to induced morbidity/mortality ( J:156696 )

• following high-intensity transverse aortic constriction compared to in similarly treated Klf5^tm2.1Rng homozygotes

increased susceptibility to xenobiotic induced morbidity/mortality ( J:156696 )

• following high-intensity transverse aortic constriction and exposure to a minimum dose of anesthetic

cardiovascular system

pulmonary vascular congestion ( J:156696 )

• following high-intensity transverse aortic constriction

abnormal myocardial fiber morphology ( J:156696 )

• following low- or high-intensity transverse aortic constriction, mice exhibit reduced cardiomyocyte hypertrophy compared with similarly treated Klf5^tm2.1Rng homozygotes

decreased heart weight ( J:156696 )

• following low- or high-intensity transverse aortic constriction compared to in similarly treated Klf5^tm2.1Rng homozygotes

cardiac hypertrophy ( J:156696 )

• following low- or high-intensity transverse aortic constriction, mice exhibit reduced cardiac hypertrophy compared with similarly treated Klf5^tm2.1Rng homozygotes

abnormal heart left ventricle morphology ( J:156696 )

• following low-intensity transverse aortic constriction, left ventricle diastolic posterior wall thickness is reduced compared to in similarly treated Klf5^tm2.1Rng homozygotes

increased heart left ventricle size ( J:156696 )

• following high-intensity transverse aortic constriction and anesthesia, one mouse exhibited increased left ventricle luminal diameter compared with similarly treated Klf5^tm2.1Rng homozygotes

cardiac interstitial fibrosis ( J:156696 )

• following low-intensity transverse aortic constriction, mice exhibit reduced cardiac interstitial fibrosis compared with similarly treated Klf5^tm2.1Rng homozygotes

abnormal cardiovascular system physiology ( J:156696 )

• following high-intensity transverse aortic constriction and anesthesia, one mouse exhibited reduced systolic function compared with similarly treated Klf5^tm2.1Rng homozygotes

abnormal myocardial fiber physiology ( J:156696 )

• following low-intensity transverse aortic constriction, mice exhibit reduced cardiomyocyte proliferation compared with similarly treated Klf5^tm2.1Rng homozygotes

abnormal response of heart to induced stress ( J:156696 )

• following low-intensity transverse aortic constriction, mice exhibit reduced cardiac hypertrophy and fibrosis, left ventricle diastolic posterior wall thickness, and cardiomyocyte hypertrophy and proliferation compared with similarly treated Klf5^tm2.1Rng homozygotes

• following high-intensity transverse aortic constriction, mice exhibit increased mortality with weight loss, rapid breathing, and pulmonary edema and/or hemorrhage but reduced cardiac hypertrophy, heart weight, and fibrosis compared with similarly treated Klf5^tm2.1Rng homozygotes

• following high-intensity transverse aortic constriction and anesthesia, one mouse exhibited enlarged left ventricle luminal diameter and reduced systolic function compared with similarly treated Klf5^tm2.1Rng homozygotes

respiratory system

pulmonary vascular congestion ( J:156696 )

• following high-intensity transverse aortic constriction

pulmonary edema ( J:156696 )

• following high-intensity transverse aortic constriction compared to in similarly treated Klf5^tm2.1Rng homozygotes

pulmonary alveolar edema ( J:156696 )

• following high-intensity transverse aortic constriction

increased wet-to-dry lung weight ratio ( J:156696 )

• following high-intensity transverse aortic constriction due to pulmonary congestion and alveolar edema

increased pulmonary respiratory rate ( J:156696 )

• following high-intensity transverse aortic constriction compared to in similarly treated Klf5^tm2.1Rng homozygotes

growth/size/body

cardiac hypertrophy ( J:156696 )

• following low- or high-intensity transverse aortic constriction, mice exhibit reduced cardiac hypertrophy compared with similarly treated Klf5^tm2.1Rng homozygotes

weight loss ( J:156696 )

• following high-intensity transverse aortic constriction compared to in similarly treated Klf5^tm2.1Rng homozygotes

homeostasis/metabolism

abnormal response of heart to induced stress ( J:156696 )

• following low-intensity transverse aortic constriction, mice exhibit reduced cardiac hypertrophy and fibrosis, left ventricle diastolic posterior wall thickness, and cardiomyocyte hypertrophy and proliferation compared with similarly treated Klf5^tm2.1Rng homozygotes

• following high-intensity transverse aortic constriction, mice exhibit increased mortality with weight loss, rapid breathing, and pulmonary edema and/or hemorrhage but reduced cardiac hypertrophy, heart weight, and fibrosis compared with similarly treated Klf5^tm2.1Rng homozygotes

• following high-intensity transverse aortic constriction and anesthesia, one mouse exhibited enlarged left ventricle luminal diameter and reduced systolic function compared with similarly treated Klf5^tm2.1Rng homozygotes

pulmonary edema ( J:156696 )

• following high-intensity transverse aortic constriction compared to in similarly treated Klf5^tm2.1Rng homozygotes

pulmonary alveolar edema ( J:156696 )

• following high-intensity transverse aortic constriction

increased susceptibility to xenobiotic induced morbidity/mortality ( J:156696 )

• following high-intensity transverse aortic constriction and exposure to a minimum dose of anesthetic

muscle

abnormal myocardial fiber morphology ( J:156696 )

• following low- or high-intensity transverse aortic constriction, mice exhibit reduced cardiomyocyte hypertrophy compared with similarly treated Klf5^tm2.1Rng homozygotes

cellular

cardiac interstitial fibrosis ( J:156696 )

• following low-intensity transverse aortic constriction, mice exhibit reduced cardiac interstitial fibrosis compared with similarly treated Klf5^tm2.1Rng homozygotes