Overview

Expression of glial fibrillary acidic protein (Gfap can be totally ablated from the jejunum and ileum in these transgeneic mice by treatment with ganciclovir, making these mice useful in studies of inflammatory bowel disease and neurogenesis.

Donating Investigator

Dr. Rene Hen, Columbia University

Christine Denny, Columbia University

Genetic overview

Genetic Background	Generation

Tg(Gfap-TK)7.1Mvs

Allele Type
Transgenic (Inserted expressed sequence)

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Research Applications

Immunology, Inflammation and Autoimmunity Research
Internal/Organ Research
Research Tools

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Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

Mice hemizygous for the transgenic insert are viable, normal in size, and do not display any behavioral abnormalities. Transgenic males are infertile. Proliferating cells that express the herpes simplex virus thymidine kinase (HSV-TK) transgene will metabolize ganciclovir (GCV) to toxic nucleotide analogues and undergo cell death. Transgene-derived HSV-TK is present exclusively in cells expressing endogenous Gfap. This coexpression occurs in brain astrocytes and adult neural stem cells, enteric glia, hepatic stellate cells, and unknown cells in heart, lung, kidney, adrenal, and spleen. Chronic GCV treatment for 21 days depletes GFAP-positive adult neural stem cells from forebrain proliferative zones. GCV treatment eliminated growth of primary multipotent neurospheres cultured from the germinal zones of postnatal and adult, but not early embryonic, transgenic mice. Notably, the same treatment prevented growth of secondary multipotent neurospheres from all three developmental stages. Stab or spinal cord injury with high dose GCV treatment for 7 days induces reactive astroctye cell death leading to altered leukocyte trafficking and impaired injury healing. High dose GCV treatment for 14 days ablates GFAP-positive glia from the jejunum and ileum leading to fulminant and fatal jejuno-ileitis. This mutant can be used instudies of adult neurogenesis, nervous system injury/repair mechanisms, and inflammatory bowel disease.

Development

A herpes simplex virus thymidine kinase (HSV-TK) construct was inserted into the first exon of a mouse glial fibrillary acidic protein (GFAP) promoter cassette (clone 445). This cassette contains all the introns, promoter regulatory elements, exons, and 2.5 kb of 5' and 2 kb of 3' flanking regions of Gfap. Transgenic Gfap expression is prevented because a small segment of exon 1 has been removed in the clone. The Gfap-HSV-Tk fusion gene was injected into the male pronucleus of fertilized eggs from superovulated female C57BL/10 x CBA mated with CFLP outbred Swiss albino males. Two-cell stage eggs were implanted into pseudopregnant foster mothers. Founder line 7.1 was obtained and backcrossed to 129S6/SvEvTac mice by the donating investigator for more than 13 generations prior to sending females and males to The Jackson Laboratory Repository.

Expression Data

Expressed Gene	HSV-TK, herpes simplex virus thymidine kinase,
Site of Expression

Control Suggestions

Noncarrier

Additional Information

Considerations for Choosing Controls

Selected References

Bush TG; Savidge TC; Freeman TC; Cox HJ; Campbell EA; Mucke L; Johnson MH; Sofroniew MV. 1998. Fulminant jejuno-ileitis following ablation of enteric glia in adult transgenic mice. Cell 93(2):189-201PubMed: 9568712 MGI: J:104241

View All References

Genetics

Tg(Gfap-TK)7.1Mvs

Allele Symbol: Tg(Gfap-TK)7.1Mvs

Allele Name	transgene insertion 7.1, Michael V Sofroniew
Allele Type	Transgenic (Inserted expressed sequence)
Allele Synonym(s)	transgene insertion 7.1, Michael V Sofroniew; Tg(Gfap-TK)7.1Mvs
Gene Symbol and Name	Tg(Gfap-TK)7.1Mvs, transgene insertion 7.1, Michael V Sofroniew
Gene Synonym(s)	Gfap-HSV-Tk; GFAP-TK
Promoter	Gfap, glial fibrillary acidic protein, mouse, laboratory
Expressed Gene	HSV-TK, herpes simplex virus thymidine kinase,
Strain of Origin	(C57BL/10 x CBA)F1 X CFLP
Chromosome	UN
General Note	Line 7.1, estimated to carry >50 copies of the transgene, was selected from three original lines (the others unnamed) for further analysis because mice of this line exhibited the greatest HSV thymidine kinase expression in the brain. Ganciclovir is metabolized to toxic nucleotide analogs in cells expressing HSV-TK. Subcutaneous or intraperitoneal administration of ganciclovir (GCV) or elaidic acid ganciclovir (eGCV) to transgenic mice results in specific ablation of proliferating cells that express GFAP.
Molecular Note	The Herpes simplex virus thymidine kinase gene, including the polyadenylation signal, was ligated into the first exon of a mouse glial fibrillary acidic protein promoter cassette that contains all the exons, introns and promoter regulatory elements and includes 2.5 kb of 5' and 2 kb of 3' flanking genomic DNA. The GFAP protein is not expressed from the transgene because a small segment of exon one has been deleted. RT-PCR analysis showed co-expression of HSV-Tk and of Gfap mRNA (from the endogenous gene) in heart, lung, liver, spleen, adrenal, kidney and GI tract, as well as in brain and trigeminal ganglion; in neural tissues the co-expressing cells have the appearance of astroglia.
Mutations Made By	Michael Sofroniew, University of California Los Angeles

Disease/Phenotype

Disease Terms

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Immunology, Inflammation and Autoimmunity Research
- Inflammation
  - Inflammatory bowel disease
- Immunodeficiency
  - Inflammatory bowel disease
Internal/Organ Research
- Wound Healing
  - delayed/impaired
- Gastrointestinal Defects
Research Tools
- Genetics Research
  - Tissue/Cell Markers
  - Tissue/Cell Markers: astrocytes, neurons
  - Tissue/Cell Markers: glial cells
  - Tissue/Cell Markers: astrocytes
- Neurobiology Research

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Tg(Gfap-TK)7.1Mvs/0
involves: C57BL/10 * CBA * CFLP

cardiovascular system phenotype

abnormal blood-brain barrier function
- days after injury
- in treated control mice and untreated transgenic mice, blood-brain barrier (BBB) is repaired and resealed by 14 days after injury where stab injury damage occurred; GCV-treated transgenics still show BBB disruption by IgG entry into CNS parenchyma at 35 days after injury

gastrointestinal hemorrhage
- ileum and jejunum of transgenics treated with GCV for >11 days exhibit hemorrhage

digestive/alimentary phenotype

abnormal crypts of Lieberkuhn morphology
- a significant 50% increase in crypt depth is seen with chronic GCV treatment
- progressive changes include crypt hyperplasia

abnormal digestive system physiology
- GCV-treated mice have a 10- to 100-fold increase in numbers of aerobic and anaerobic bacterial colonies per gram tissue in ileum compared to untreated or GVC-treated nontransgenic mice
- transgenic mice receiving 100 mg/kg/day GCV for 14 show growth of gram-negative organisms (>300 colonies per spleen or ml of blood or peritoneal fluid) while controls have none

abnormal feces composition
- the fecal contents of transgenic mice given GCV for >11 days are black, melanic and test positive for occult blood

abnormal ileum morphology
- ileum of affected mice is generally more severely affected than jejunum; lesions occur with equal frequency within the proximal, central or distal portions
- some areas of severely affected ileal mucosa is associated with necrosis of the underlying smooth muscle and transmural perforation
- the smooth muscle wall of the ileum shows an obvious 100% thickening

abnormal intestinal goblet cell morphology
- some treated animals with severe pathology show loss of goblet cells

abnormal intestinal mucosa morphology
- lamina propria becomes inflamed in affected mice; fibrosis of, and hemorrhage into lamina propria can be seen in severe cases
- progressive changes include increased sloughing of epithelial cells
- surface exhibits areas of superficial erosion covered with inflammatory exudates and cellular debris
- surface exhibits areas of superficial erosion covered with inflammatory exudates and cellular debris in trangenics after chronic GCV treatment
- villi in severely affected regions can show disintegration of the tips resulting in a hemorrhagic and inflammatory exudates into the lumen of intestine
- villus atrophy is minor, but villi exhibit patchy lesions ranging from mild epithelial changes and nonspecific granulocytic infiltrate to marked hemorrhagic necrosis
- villus tips show flattening, vacuolization and loss of polarity of surface epithelium; loss of brush border and pronounced dilation of capillaries with erythrostasis with chronic GCV treatment

abnormal jejunum morphology
- jejunum of GCV-treated mice displays similar pathology to the ileum, but usually with less severity

abnormal small intestine morphology
- ileum and jejunum of transgenics treated with GCV (100 mg/kg/day) for >11 days exhibit moderate distention
- inflammation and hemorrhagic necrosis of the submucosa and muscularis externa can be seen in severely affected regions
- small intestine shows patchy skip lesions ranging from small inflammatory foci to large apthoid and linear ulcers exhibiting gangrenous necrosis in extreme cases

distended ileum
- ileum of transgenics treated with GCV (100 mg/kg/day) for >11 days exhibits moderate distention

distended jejunum
- jejunum of transgenics treated with GCV (100 mg/kg/day) for >11 days exhibits moderate distention

gastrointestinal hemorrhage
- ileum and jejunum of transgenics treated with GCV for >11 days exhibit hemorrhage

small intestinal inflammation
- ileum and jejunum of transgenics treated with GCV for >11 days show severe inflammation
- progression changes in inflammation lead to increased transmigration of polymorphonuclear leukocytes leading to granulocytic inflammatory infiltrate of lamina propria

endocrine/exocrine gland phenotype

abnormal crypts of Lieberkuhn morphology
- a significant 50% increase in crypt depth is seen with chronic GCV treatment
- progressive changes include crypt hyperplasia

hematopoietic system phenotype

anemia
- moribund treated transgenics display severe anemia

decreased erythrocyte cell number
- transgenic mice receiving 100 mg/kg/day GCV for 14 days have red blood cell counts reduced by 60%

increased neutrophil cell number
- moribund treated transgenics have a high level of neutrophils relative to the number of red blood cells
- transgenic mice receiving 100 mg/kg/day GCV for 14 days show 20-fold increase in neutrophils

increased nucleated erythrocyte cell number
- moribund treated transgenics have high levels of nucleated red blood cells
- transgenic mice receiving GCV for 14 days show a 10-fold increase in nucleated red blood cells

cellular phenotype

abnormal cell death
- in enriched subconfluent astrocyte cultures from neonatal mice, exposure to GCV for 7 days or more caused a 75% loss of astrocytes (GFAP +ve cells) with an increase in GFAP -ve cells compared to nontransgenic cultures

abnormal cell proliferation
- non-transgenic animals with or without GCV treatment show many proliferating astrocytes in narrow zone adjacent to stab wound associated with compact glial scar formation, but in GCV-treated mutants, essentially all proliferating astrocytes are ablated

abnormal intestinal goblet cell morphology
- some treated animals with severe pathology show loss of goblet cells

abnormal neuron differentiation
- in transgenic mice treated daily with low-dose ganciclovir (GCV), number of dividing cells decreases substantially in subependymal zone (SEZ) to 18.6% of controls and in subgranular zone (SGZ) to 29.6% of control
- o controls (>98% reduction in neurogenesis)
- transgenic mice treated chronically (14 days) with low-dose GCV have almost no newly generated neurons in SEZ, SGZ, or rostral migratory stream (RMS); in olfactory bulb 0% of neurons are NeuN-positive and in dentate gyrus only 1.8% are positive compared to controls (>98% reduction in neurogenesis)

increased susceptibility to neuronal excitotoxicity
- many CA1 neurons in GCV-treated mice show morphological signs of excitotoxic cell death, compared to control mice

homeostasis/metabolism phenotype

abnormal enzyme/coenzyme activity
- in GCV-treated transgenic mice, a substantial increase in myeloperoxidase (MPO) activity, a quantitative measure of inflammatory response, in ileum not duodenum or colon compared to nontransgenic mice

decreased sensitivity to xenobiotic induced morbidity/mortality
- untreated nontransgenic mice show no effects beyond reduced activity and ruffled fur after 28 days of 100 mg/kg/day ganciclovir (GCV) treatment
- when treated with GCV up to 7 days, mice survive for at least 35 days; when treated for 14 days then stopped, mice become terminally ill and death occurs between 13 and 19 days (100% mortality) with or without a brain injury

edema
- in some affected mice, interstitial edema separating the epithelium from the lamina propria is observed

impaired wound healing
- GCV-treated transgenic mice show reactive astrocyte death and impaired glial scar formation after stab injury to the brain

increased blood urea nitrogen level
- moribund treated transgenics have 3-fold elevated serum urea levels compared to untreated controls
- transgenic mice receiving GCV for 14 days have mildly (30%) elevated serum urea levels

increased susceptibility to neuronal excitotoxicity
- many CA1 neurons in GCV-treated mice show morphological signs of excitotoxic cell death, compared to control mice

immune system phenotype

abnormal inflammatory response
- transgenic mice given 100 mg/kg/day GCV for 7 days show small patches of focal inflammation in the GI tract

brain inflammation
- blood vessels are dilated, a 25-fold greater density of leukocytes are present and persist for 14 days, and extravasated leukocytes (monocytes, macrophages, neutrophils, and lymphocytes) are common up to 2 mm from wound
- in GCV-treated mutants, at 7 days after stab injury, there is marked interstitial edema within 400 microns of wound with numerous phagocytic and inflammatory cells and substantial neuronal degeneration
- many microglia are seen adjacent to wound at 7 or 14 days and at 35 days, numerous leukocytes are still observed, while non-transgenic GCV-treated and transgenic untreated show little edema, a low density of leukocytes scattered around wound, and extravasated monocytes are rarely found in parenchyma at >1 mm from wound margin
- sated monocytes are rarely found in parenchyma at >1 mm from wound margin

increased neutrophil cell number
- moribund treated transgenics have a high level of neutrophils relative to the number of red blood cells
- transgenic mice receiving 100 mg/kg/day GCV for 14 days show 20-fold increase in neutrophils

small intestinal inflammation
- ileum and jejunum of transgenics treated with GCV for >11 days show severe inflammation
- progression changes in inflammation lead to increased transmigration of polymorphonuclear leukocytes leading to granulocytic inflammatory infiltrate of lamina propria

mammalian phenotype

nervous system phenotype
- Normal - uninjured transgenic mice receiving 100 mg/kg/day GCV for 14-17 days show no evidence of neuronal damage or astrocyte loss throughout the CNS

mortality/aging

decreased sensitivity to xenobiotic induced morbidity/mortality
- untreated nontransgenic mice show no effects beyond reduced activity and ruffled fur after 28 days of 100 mg/kg/day ganciclovir (GCV) treatment
- when treated with GCV up to 7 days, mice survive for at least 35 days; when treated for 14 days then stopped, mice become terminally ill and death occurs between 13 and 19 days (100% mortality) with or without a brain injury

nervous system phenotype

abnormal astrocyte physiology
- after a stab injury to brain and continuous GCV delivery in vivo for 7 or 14 days, transgenic mice show few astrocytes adjacent to wound margin and astrocytes in adjacent tissue look fragmented and abnormal (early stages of cell death)
- transgenic astrocytes are sensitive to prolonged exposure to subcutaneous GCV, resulting in cell death

abnormal blood-brain barrier function
- days after injury
- in treated control mice and untreated transgenic mice, blood-brain barrier (BBB) is repaired and resealed by 14 days after injury where stab injury damage occurred; GCV-treated transgenics still show BBB disruption by IgG entry into CNS parenchyma at 35 days after injury

abnormal CNS glial cell morphology
- after a stabbing injury to the forebrain, transgenic mice treated with ganciclovir (GCV) subcutaneously for 7 or 14 days show a reduction in astrocytes immediately adjacent to wound and for several hundred microns away, most strikingly the thalamus

abnormal enteric nervous system morphology
- after 14 days of GCV treatment, transgenic mice show pronounced loss of glial (GFAP +ve) cells from myenteric plexus in jejunum and ileum; widespread loss from submucosal regions and lamina propria of villi throughout jejunum and ileum is seen

abnormal enteric neuron morphology
- in areas where many glial cells are absent, neuronal atrophy and loss can be observed
- in transgenics after GCV treatment there are 31% fewer myenteric neurons and remaining neurons have a 27% smaller mean cross-sectional area
- the dense network of glial cell processes that envelop the myenteric neurons in controls is markedly depleted in transgenic mice receiving GCV for 14 days

abnormal glial cell morphology
- remaining enteric glia after 14 days of GCV treatment are abnormal

abnormal innervation
- GCV-treated mutants show a dense network of many finely branched, randomly-oriented fibers with a sprouting appearance comfined to the wound margin and not extending into unaffected regions while control mice show very few fibers in scar-forming region

abnormal neuron differentiation
- in transgenic mice treated daily with low-dose ganciclovir (GCV), number of dividing cells decreases substantially in subependymal zone (SEZ) to 18.6% of controls and in subgranular zone (SGZ) to 29.6% of control
- o controls (>98% reduction in neurogenesis)
- transgenic mice treated chronically (14 days) with low-dose GCV have almost no newly generated neurons in SEZ, SGZ, or rostral migratory stream (RMS); in olfactory bulb 0% of neurons are NeuN-positive and in dentate gyrus only 1.8% are positive compared to controls (>98% reduction in neurogenesis)

astrocytosis
- death of astrocytes immediately next to the wound triggers extensive astrocytosis in outwardly adjacent cells compared to controls

brain inflammation
- blood vessels are dilated, a 25-fold greater density of leukocytes are present and persist for 14 days, and extravasated leukocytes (monocytes, macrophages, neutrophils, and lymphocytes) are common up to 2 mm from wound
- in GCV-treated mutants, at 7 days after stab injury, there is marked interstitial edema within 400 microns of wound with numerous phagocytic and inflammatory cells and substantial neuronal degeneration
- many microglia are seen adjacent to wound at 7 or 14 days and at 35 days, numerous leukocytes are still observed, while non-transgenic GCV-treated and transgenic untreated show little edema, a low density of leukocytes scattered around wound, and extravasated monocytes are rarely found in parenchyma at >1 mm from wound margin
- sated monocytes are rarely found in parenchyma at >1 mm from wound margin

increased susceptibility to neuronal excitotoxicity
- many CA1 neurons in GCV-treated mice show morphological signs of excitotoxic cell death, compared to control mice

loss of hippocampal neurons
- GCV-treated mice by 21 or 35 days after stab injury show few surviving pyramidal neurons within 1500 microns of wound and extensive tissue collapse; in control mice, region with no neurons extends <100 microns from the wound
- loss of neurons is seen in all brain tissue around the stab injury in GCV-treated transgenics

neuron degeneration
- loss of enteric glia results in a patchy, moderate degeneration of neurons intrinsic to the ileal myenteric plexus
- marked degeneration in the wound region is observed 7 days after injury in GCV-treated transgenics

reproductive system phenotype

male infertility
- male transgenic mice are sterile

References

Bush TG; Savidge TC; Freeman TC; Cox HJ; Campbell EA; Mucke L; Johnson MH; Sofroniew MV. 1998. Fulminant jejuno-ileitis following ablation of enteric glia in adult transgenic mice. Cell 93(2):189-201PubMed: 9568712 MGI: J:104241

Additional - Tg(Gfap-TK)7.1Mvs related

Technical Support

Contact Technical Support

Genotyping Protocols
- Standard PCR: Tg(Gfap-Tk)7.1Mvs
- MELT: Tg(Gfap-TK)7.1Mvs Alternate2
- Genotyping resources and troubleshooting
Breeding Considerations

Transgenic males are infertile. When maintaining a live colony, hemizygous females are bred to wildtype (noncarrier) males.
- Additional Breeding and Husbandry Support
Citation
When using the 129S6.Cg-Tg(Gfap-TK)7.1Mvs/RhnJ mouse strain in a publication, please cite the originating article(s) and include JAX stock #017523 in your Materials and Methods section.

Animal Health Reports

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Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Pricing & Availability

Cryo Recovery

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service	Genotype	Price
	Heterozygous females and wildtype males for Tg(Gfap-TK)7.1Mvs

We will fulfill your order by providing at least two carriers for each strain ordered. The total number, sex, and genotypes provided will vary, although typically 8 or more animals are provided. Please check genotypes which will be recovered. While the genotypes of all animals produced will be communicated to you prior to scheduling shipment, the genotypes of animals provided may not reflect the mating scheme and genotypes described in the strain description. Animals are typically ready to ship in 11-14 weeks. If a second recovery is required to produce the minimum number of animals, then delivery time would increase to approximately 25 weeks. If we fail to produce animals of the correct genotype, you will not be charged. We cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation.

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Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Expression Data

Control Suggestions

Additional Information

Selected References

Tg(Gfap-TK)7.1Mvs

Allele Symbol: Tg(Gfap-TK)7.1Mvs

Disease Terms

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Mammalian Phenotype Terms by Genotype

Genotype: Tg(Gfap-TK)7.1Mvs/0involves: C57BL/10 * CBA * CFLP

cardiovascular system phenotype

digestive/alimentary phenotype

endocrine/exocrine gland phenotype

hematopoietic system phenotype

cellular phenotype

homeostasis/metabolism phenotype

immune system phenotype

mammalian phenotype

mortality/aging

nervous system phenotype

reproductive system phenotype

References

Additional - Tg(Gfap-TK)7.1Mvs related

Genotyping Protocols

Breeding Considerations

Citation

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Live Mouse

Cryorecovery - Pricing

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms of Use

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Genotype: Tg(Gfap-TK)7.1Mvs/0
involves: C57BL/10 * CBA * CFLP