Overview

Also Known As:B6-tight skin

Estimated Removal of Live Colony date: 16 July 2020.

Fbn1^Tsk homozygotes are embryonic lethal; heterozygotes exhibit excessive growth and hyperplasia of connective tissue, cartilage, tendon sheaths and bone. This strain is a model for Marfan Syndrome, Hereditary Pulmonary Emphysema, Stiff Skin Syndrome and Familial Progressive Scleroderma.

Donating Investigator

IMR Colony, The Jackson Laboratory

Genetic overview

Genetic Background	Generation

Fbn1^Tsk

Allele Type	Gene Symbol	Gene Name
Spontaneous	Fbn1	fibrillin 1

View Genetics

Research Applications

Internal/Organ Research
Mouse/Human Gene Homologs
Dermatology Research
Developmental Biology Research
Immunology, Inflammation and Autoimmunity Research
Research Tools
Cell Biology Research
Cardiovascular Research

View All Research Applications

Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

The Fbn1^Tsk allele contains a 30 to 40 kbp genomic tandem duplication resulting in a larger than normal in-frame transcript. Homozygotes are embryonic lethal, failing to survive past somite formation (7-8 days of gestation). Heterozygotes are viable and fertile, exhibiting excessive growth and hyperplasia of connective tissue, cartilage, tendon sheaths and bone. Skin tightness, due to hyperplasic thickening of subcutaneous loose connective tissue and abnormal organization and distribution of skin microfibrillar arrays, develops by the first week after birth. Although the size of the skeleton is increased, body weight remains normal. Mutant mice exhibit polyuria during the light cycle. Collagens and glycosaminoglycans accumulate in the skin, heart, lungs and bladder. Hypertrophy is also observed in the enlarged heart (aortic adventitia). Mutant mice have enlarged thoracic size and lungs with abnormal alveolar walls, irregular shaped alveoli, and increased lung capacity. By 1 month of age, heterozygotes develop emphysema with progressive destruction of alveolar walls and loss of elasticity. Inflammatory macrophages and neutrophils infiltrate the lower respiratory tract. The abnormal immune system characteristics exhibited by this strain also include: alveolitis, increased number of mast cells in the skin, presence of autoantibodies specific for scleroderma target antigens and anti-nuclear antibodies.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Development

The spontaneous mutation Fbn1^Tsk (tight skin) arose in 1977 at The Jackson Laboratory from the B10.D2(58N) congenic resistant strain.

This strain was generated by breeding B6.Cg-Fbn1^Tsk +/+ Bloc1s6^pa/J (Stock No. 000305) to C57BL6/J (Stock No. 000664) to remove the Bloc1s6^pa allele.

A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, 4 of 5 markers that determine C57BL/6J from C57BL/6N were found to be segregating. These data suggest the mice sent to The Jackson Laboratory Repository were on a mixed C57BL/6J ; C57BL/6N genetic background.

Control Suggestions

Wild-type from the colony
000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

Akita M; Lee SH; Kaneko K. 1992. Electron microscopic observations of elastic fibres in the lung and aorta of tight-skin and beta-aminopropionitrile-fed mice. Histol Histopathol 7(1):39-45PubMed: 1576433 MGI: J:1326
Green MC; Sweet HO. 1973. Tight skin (Tsk) Mouse News Lett 48:34MGI: J:27521
Green MC; Sweet HO; Bunker LE. 1976. Tight-skin, a new mutation of the mouse causing excessive growth of connective tissue and skeleton. Am J Pathol 82(3):493-512PubMed: 176891 MGI: J:5629
Rossi GA; Hunninghake GW; Gadek JE; Szapiel SV; Kawanami O; Ferrans VJ; Crystal RG. 1984. Hereditary emphysema in the tight-skin mouse. Evaluation of pathogenesis. Am Rev Respir Dis 129(5):850-5PubMed: 6562869 MGI: J:15018
Siracusa LD; McGrath R; Ma Q; Moskow JJ; Manne J; Christner PJ; Buchberg AM; Jimenez SA. 1996. A tandem duplication within the fibrillin 1 gene is associated with the mouse tight skin mutation. Genome Res 6(4):300-13PubMed: 8723723 MGI: J:32931
Szapiel SV; Fulmer JD; Hunninghake GW; Elson NA; Kawanami O; Ferrans VJ; Crystal RG. 1981. Hereditary emphysema in the tight-skin (Tsk/+) mouse. Am Rev Respir Dis 123(6):680-5PubMed: 7271067 MGI: J:6566

View All References

Genetics

Fbn1^Tsk

Allele Symbol: Fbn1^Tsk

Allele Name	tight skin
Allele Type	Spontaneous
Allele Synonym(s)	TSK
Gene Symbol and Name	Fbn1, fibrillin 1
Gene Synonym(s)
Strain of Origin	B10.D2/(58N)Sn
Chromosome	2
General Note	Genbank ID for this allele: AF007248
Molecular Note	This allele harbors a 30 to 40kb genomic tandem duplication within the Fbn1 gene that results in a larger than normal in-frame transcript produced at normal levels.

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

Marfan syndrome

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

Research Areas By Phenotype

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

Genotype: Fbn1^Tsk related

Internal/Organ Research
- Lung Defects
  - emphysema
Mouse/Human Gene Homologs
- Marfan syndrome
Dermatology Research
- Skin and Hair Texture Defects
Developmental Biology Research
- Defects in Extracellular Matrix Molecules

Internal/Organ Research
- Lung Defects
  - emphysema
- Skeleton
  - Bone
Dermatology Research
- Skin and Hair Texture Defects
Developmental Biology Research
- Embryonic Lethality (Homozygous)
- Skeletal Defects
- Growth Defects
Immunology, Inflammation and Autoimmunity Research
- Autoimmunity
- Inflammation
Research Tools
- Cardiovascular Research
- Immunology, Inflammation and Autoimmunity Research
Cell Biology Research
- Genes Regulating Growth and Proliferation
Cardiovascular Research
- Heart Abnormalities

Mammalian Phenotype Terms by Genotype

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

Genotype: Fbn1^Tsk/Fbn1⁺
B10.D2/(58N)Sn

behavior/neurological phenotype

hunched posture
- develop a pronounced hump in the shoulder region and hunched posture with age

integument phenotype

abnormal dermal layer morphology
- collagen fibrils within the fascicles of the dermis are less ordered and the fascicles are thinner and more closely packed and appear to bend and twist more along their course
- dermis fibroblasts often contain greatly distended rough endoplasmic reticulum cisternae

abnormal dermis papillary layer morphology
- fibrous organization of collagen fibrils is not distinctly visible in the hyalinized areas of the superficial dermis

abnormal hypodermis morphology
- fascicles of unusually thin collagen fibrils are found in scattered areas of the hypodermis
- hyperplasia of the subcutaneous loose connective tissue
- hypodermis is more lamellar
- in loose connective tissue, exhibit large accumulations of microfibrils in the intercellular space

abnormal skin condition

abnormal skin morphology

thick dermal layer
- reticular dermis of skin is consistently thicker and often more cellular than that of wild-type

thick hypodermis
- hypodermis is substantially thicker

tight skin
- caused by hyperplasia of subcutaneous loose connective tissue
- skin is firmly bound to subcutaneous and deep muscular tissue
- skin lacks normal pliability and elasticity
- skin tightness is not seen at birth but develops during the first postnatal week

cardiovascular system phenotype

cardiac hypertrophy

dilated heart atrium

dilated heart right ventricle
- enlarged but not as much as the auricles

enlarged heart

muscle phenotype

abnormal tendon morphology
- in older mice, some tendons show degenerative changes with increased cellularity and decreased amount of collagen
- small tendons with hyperplasia of tendon sheaths or with accumulation of fluid within the sheath

abnormal tendon sheath morphology
- ankle tendons show hyperplasia of the tendon sheath as well as hyperplasia of the loose connective tissue between the tendons
- in the tail, tendon size reduction is often associated with hyperplasia of the tendon sheath or with accumulation of fluid with the sheath

respiratory system phenotype

abnormal lung morphology
- lungs become abnormally distended in enlarged thorax

abnormal tracheal cartilage morphology
- longer length of the fourth tracheal ring

emphysema
- vesicular emphysema

skeleton phenotype

abnormal cartilage morphology
- increase in growth of cartilage
- longer length of the ear cartilage

abnormal costal cartilage morphology
- costal cartilages are elongated and more bowed than normal

abnormal pelvic girdle bone morphology
- pelvic bone is about 10% larger

abnormal skeleton morphology
- excessive growth of connective tissue and skeleton
- increase in skeletal size, however body weight is not increased

abnormal tendon morphology
- in older mice, some tendons show degenerative changes with increased cellularity and decreased amount of collagen
- small tendons with hyperplasia of tendon sheaths or with accumulation of fluid within the sheath

abnormal tendon sheath morphology
- ankle tendons show hyperplasia of the tendon sheath as well as hyperplasia of the loose connective tissue between the tendons
- in the tail, tendon size reduction is often associated with hyperplasia of the tendon sheath or with accumulation of fluid with the sheath

abnormal tracheal cartilage morphology
- longer length of the fourth tracheal ring

enlarged cranium
- longer skull

enlarged lumbar vertebrae
- enlarged in both length and width

increased length of long bones
- long bones and girdles are about 5% larger

long mandible
- longer and wider mandible

long ribs
- longer ribs

craniofacial phenotype

enlarged cranium
- longer skull

long mandible
- longer and wider mandible

growth/size/body region phenotype

cardiac hypertrophy

enlarged heart

enlarged thoracic cavity
- enlarged thorax causing distension of the thoracic viscera

Genotype: Fbn1^Tsk/Fbn1^Tsk
B10.D2/(58N)Sn

mortality/aging

embryonic lethality between implantation and somite formation, complete penetrance
- die at 7-8 days of gestation

Genotype: Fbn1^Tsk/Fbn1⁺
B6.Cg-Fbn1 +/+ Bloc1s6/JKcc

cardiovascular system phenotype

abnormal aorta elastin content
- in 3 week old mice fragmentation of elastic lamellae is seen in van-Gieson stained histological sections of the ascending aorta

integument phenotype

abnormal dermal layer morphology

abnormal dermis reticular layer collagen network
- Trichrome-stained sections of adult skin show loose connective tissue contains excessive collagen fibers tightly bound to the muscle layer

abnormal dermis reticular layer morphology
- Trichrome-stained sections of adult skin show loose connective tissue contains excessive collagen fibers tightly bound to the muscle layer

The following phenotype relates to a compound genotype created using this strain

Genotype: Fbn1^Tsk/Fbn1⁺
B6.Cg-Fbn1

cardiovascular system phenotype

abnormal aorta tunica adventitia morphology
- aorta exhibits hyperplasia of loose connective tissue in the adventitia
- collagen fibers in the aorta are increased and microfibrils surrounding elastin in the adventitia of the aorta are not clearly apparent

abnormal heart morphology
- 2.5-fold increase in type VI collagen content in myocardium
- collagen deposition is increased in the heart
- type I collagen is increased in the myocardium, perhaps due to reduced activity of negative regulatory sequence

abnormal heart right ventricle morphology
- an increase in collagen content
- increase in collagen content in the right ventricle at 3 months of age; however, by 16 months of age, collagen content returns to normal levels but there is a shift in collagen type due to an increase in type I collagen, and by 24 months of age, again see an increase in collagen content

cardiac fibrosis
- exhibit myocardial fibrosis
- thyroid hormone treatment decreases collagen synthesis and stimulates regression of cardiac fibrosis

heart right ventricle hypertrophy
- starts to develop at around 8 months of age

embryo phenotype

abnormal uterine NK cell morphology
- distribution of granulated metrial gland cells, a uterine natural killer-like cell subset, is abnormal during pregnancy, with cells seen in the antimesometral and lateral decidual regions at E8.5 and in regions between implantation sites until E10.5, however their differentiation progresses normally
- ver their differentiation progresses normally

endocrine/exocrine gland phenotype

abnormal uterine NK cell morphology
- distribution of granulated metrial gland cells, a uterine natural killer-like cell subset, is abnormal during pregnancy, with cells seen in the antimesometral and lateral decidual regions at E8.5 and in regions between implantation sites until E10.5, however their differentiation progresses normally
- ver their differentiation progresses normally

growth/size/body region phenotype

heart right ventricle hypertrophy
- starts to develop at around 8 months of age

hematopoietic system phenotype

abnormal uterine NK cell morphology
- distribution of granulated metrial gland cells, a uterine natural killer-like cell subset, is abnormal during pregnancy, with cells seen in the antimesometral and lateral decidual regions at E8.5 and in regions between implantation sites until E10.5, however their differentiation progresses normally
- ver their differentiation progresses normally

increased mast cell number
- increase in number and enhanced degree of degranulation of mast cells in the skin

immune system phenotype

abnormal uterine NK cell morphology
- distribution of granulated metrial gland cells, a uterine natural killer-like cell subset, is abnormal during pregnancy, with cells seen in the antimesometral and lateral decidual regions at E8.5 and in regions between implantation sites until E10.5, however their differentiation progresses normally
- ver their differentiation progresses normally

alveolitis
- exhibit alveolitis, with increased numbers of alveolar macrophages and neutrophils in the alveolar lumens
- macrophage-neutrophil alveolitis is seen at 3 weeks of age, at a time when emphysematous lesions are not yet present
- presence of focal collections of mononuclear phagocytes, lymphocytes, and neutrophils within alveolar air spaces

increased autoantibody level
- develop anti-nucleolar antibodies and produce significantly higher titers of autoantibodies specific for scleroderma target antigens (topo I, RNA pol I, and Fc gamma R)
- develop autoantibodies specific for scleroderma target antigens, with a bias toward the use of V_HJ558 genes and J_H2 and J_K2 segments

increased mast cell number
- increase in number and enhanced degree of degranulation of mast cells in the skin

increased susceptibility to type IV hypersensitivity reaction
- develop cell-mediated immunity to elastase-soluble murine lung peptides with age while delayed-type hypersensitivity responses to type I or type IV collagen are not detected

lung inflammation
- increased numbers of alveolar macrophages and neutrophils in the interstitium
- presence of focal collections of mononuclear phagocytes, lymphocytes, and neutrophils in the interstitium

integument phenotype

abnormal cutaneous collagen fibril morphology
- electron micrographs of skin show a predominance of abnormally small diameter collagen fibers and the skin shows abundant irregular and wavy collagen bundles

abnormal cutaneous microfibril morphology
- although there is a morphologically normal population of skin microfibrils, approximately 45% of the skin microfibril population has abnromal periodic arrays of beads with indistinct filamentous interbeads and extended periodicity of 112 (+/-11) nm relative to 55 (+/-4) nm in normal microfibrils
- egates fail to dissociate
- the abnormal skin microfibrils have an altered response to calcium chelation by EDTA, with diminished shortening of the periodicity of microfibrils and less prominant appearance of beading compared with control microfibrils, and the large microfibril aggregates fail to dissociate
- transmission electron microscopy of the upper dermis shows more prominent microfibrillar clusters, which often appear blurred and lacking a discernible striated pattern, but an absence of well-packed elastic fibrils
- ve to 55 (+/-4) nm in normal microfibrils

abnormal hypodermis morphology
- increase in width of the subcutaneous fibrous layer with increasing age

abnormal skin morphology
- hexosamine, uronic acid, and total glycosaminoglycan content is increased in skin
- significantly greater skin biopsy weights, however percent of water-fat is similar to wild-type

abnormal skin physiology
- cultured skin fibroblasts synthesize almost 5 times more Type I and Type III procollagen mRNA indicating production of excessive amounts of collagen
- fibroblasts synthesize increased collagen both constitutively and in response to IL4 or TGFB, although IL13 does not increase fibroblast collagen synthesis

skin fibrosis
- develop skin fibrosis which results originally from collagen I and III overexpression and later collagen VI overexpression
- unlike human scleroderma, fibrosis does not manifest Tgfb1 mRNA in areas of abnormal collagen deposition

thick skin
- skin is 228 um thick on average instead of the wildtype 132 um

mammalian phenotype

homeostasis/metabolism phenotype
- Normal - no aberrant bleeding time after tail vein nick

muscle phenotype

heart right ventricle hypertrophy
- starts to develop at around 8 months of age

renal/urinary system phenotype

abnormal urinary bladder morphology
- 70% increase in collagen content and concentration in the bladder at 5-6 months of age

abnormal urinary bladder physiology
- functional bladder capacity appears to be greater

polyuria
- urinate larger volumes more frequently during the light cycle

reproductive system phenotype

abnormal uterine NK cell morphology
- distribution of granulated metrial gland cells, a uterine natural killer-like cell subset, is abnormal during pregnancy, with cells seen in the antimesometral and lateral decidual regions at E8.5 and in regions between implantation sites until E10.5, however their differentiation progresses normally
- ver their differentiation progresses normally

respiratory system phenotype

abnormal alveolar pore morphology
- alveolar pores in septa are variable in size and increased in number
- increase in the number and size of the pores of Kohn

abnormal bronchiole morphology
- dilation of bronchioles

abnormal lung morphology

abnormal pulmonary alveolus morphology
- alveoli are irregular in size, with most appearing enlarged
- at 3 weeks of age, alveoli are flattened but not enlarged, however by 4-6 weeks af age, alveoli are enlarged
- enlargement of air spaces with numerous subpleural cysts and scattered bullae
- exhibit formation of bullae and subpleural cysts and fragmented elastin in alveolar walls
- numerous broken alveolar septa and bullous lesions
- thinning and destruction of alveolar walls

abnormal pulmonary alveolus wall morphology
- thinning and destruction of alveolar walls

abnormal pulmonary interalveolar septum morphology
- progressive destruction of alveolar septa and increase in collagen deposition in the septa that may result from repair of the lung destruction

alveolitis
- exhibit alveolitis, with increased numbers of alveolar macrophages and neutrophils in the alveolar lumens
- macrophage-neutrophil alveolitis is seen at 3 weeks of age, at a time when emphysematous lesions are not yet present
- presence of focal collections of mononuclear phagocytes, lymphocytes, and neutrophils within alveolar air spaces

dilated pulmonary alveolar ducts
- dilation of alveolar ducts
- enlarged alveolar ducts are first seen at 3 weeks of age

emphysema
- emphysematous lesions are seen at 4 weeks of age

increased lung compliance
- increase in lung compliance

increased total lung capacity
- increase in total lung capacity

lung inflammation
- increased numbers of alveolar macrophages and neutrophils in the interstitium
- presence of focal collections of mononuclear phagocytes, lymphocytes, and neutrophils in the interstitium

overexpanded pulmonary alveoli
- develop enlarged alveoli between 4 and 6 weeks of age
- distension of many alveoli
- enlarged alveoli are 3 to 4 times larger than normal and show a histologic picture of emphysema

thick pulmonary interalveolar septum
- diffuse thickening of the septa not affected by emphysematous changes, resulting from a progressive increase in collagen

References

Akita M; Lee SH; Kaneko K. 1992. Electron microscopic observations of elastic fibres in the lung and aorta of tight-skin and beta-aminopropionitrile-fed mice. Histol Histopathol 7(1):39-45PubMed: 1576433 MGI: J:1326
Green MC; Sweet HO. 1973. Tight skin (Tsk) Mouse News Lett 48:34MGI: J:27521
Green MC; Sweet HO; Bunker LE. 1976. Tight-skin, a new mutation of the mouse causing excessive growth of connective tissue and skeleton. Am J Pathol 82(3):493-512PubMed: 176891 MGI: J:5629
Rossi GA; Hunninghake GW; Gadek JE; Szapiel SV; Kawanami O; Ferrans VJ; Crystal RG. 1984. Hereditary emphysema in the tight-skin mouse. Evaluation of pathogenesis. Am Rev Respir Dis 129(5):850-5PubMed: 6562869 MGI: J:15018
Siracusa LD; McGrath R; Ma Q; Moskow JJ; Manne J; Christner PJ; Buchberg AM; Jimenez SA. 1996. A tandem duplication within the fibrillin 1 gene is associated with the mouse tight skin mutation. Genome Res 6(4):300-13PubMed: 8723723 MGI: J:32931
Szapiel SV; Fulmer JD; Hunninghake GW; Elson NA; Kawanami O; Ferrans VJ; Crystal RG. 1981. Hereditary emphysema in the tight-skin (Tsk/+) mouse. Am Rev Respir Dis 123(6):680-5PubMed: 7271067 MGI: J:6566

Additional - Fbn1^Tsk related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Fbn1
- Genotyping resources and troubleshooting
Breeding Considerations

Homozygotes are not viable. When maintaining a live colony, C57BL/6J female mice may be bred with heterozygous male mice.
- Additional Breeding and Husbandry Support
Mating System
- C57BL/6J (000664) x Heterozygote
Appearance
- Hair loss has been observed in this colony.
Citation
When using the B6-tight skin mouse strain in a publication, please cite the originating article(s) and include JAX stock #014632 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

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/Product	Description	Price
	Heterozygous or Wildtype for Fbn1<Tsk>

Related Products and Services

Frozen Mouse Embryo	B6.Cg-Fbn1<Tsk>/J	$2595.00
Frozen Mouse Embryo	B6.Cg-Fbn1<Tsk>/J	$2595.00
Frozen Mouse Embryo	B6.Cg-Fbn1<Tsk>/J	$3373.50
Frozen Mouse Embryo	B6.Cg-Fbn1<Tsk>/J	$3373.50

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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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Also Known As:B6-tight skin

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Fbn1Tsk

Allele Symbol: Fbn1Tsk

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

Research Areas By Phenotype

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

Genotype: Fbn1Tsk related

Mammalian Phenotype Terms by Genotype

Genotype: Fbn1Tsk/Fbn1+B10.D2/(58N)Sn

behavior/neurological phenotype

integument phenotype

cardiovascular system phenotype

muscle phenotype

respiratory system phenotype

skeleton phenotype

craniofacial phenotype

growth/size/body region phenotype

Genotype: Fbn1Tsk/Fbn1TskB10.D2/(58N)Sn

mortality/aging

Genotype: Fbn1Tsk/Fbn1+B6.Cg-Fbn1 +/+ Bloc1s6/JKcc

cardiovascular system phenotype

integument phenotype

Genotype: Fbn1Tsk/Fbn1+B6.Cg-Fbn1

cardiovascular system phenotype

embryo phenotype

endocrine/exocrine gland phenotype

growth/size/body region phenotype

hematopoietic system phenotype

immune system phenotype

integument phenotype

mammalian phenotype

muscle phenotype

renal/urinary system phenotype

reproductive system phenotype

respiratory system phenotype

References

Additional - Fbn1Tsk related

Genotyping Protocols

Breeding Considerations

Mating System

Appearance

Citation

Animal Health Reports

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

Live Mouse

Cryorecovery - Pricing

Related Products and Services

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

Fbn1^Tsk

Allele Symbol: Fbn1^Tsk

Genotype: Fbn1^Tsk related

Genotype: Fbn1^Tsk/Fbn1⁺
B10.D2/(58N)Sn

Genotype: Fbn1^Tsk/Fbn1^Tsk
B10.D2/(58N)Sn

Genotype: Fbn1^Tsk/Fbn1⁺
B6.Cg-Fbn1 +/+ Bloc1s6/JKcc

Genotype: Fbn1^Tsk/Fbn1⁺
B6.Cg-Fbn1

Additional - Fbn1^Tsk related