Strain Name:

STOCK Tgfb2tm1Doe/J

Stock Number:

003102

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Availability:

Cryopreserved - Ready for recovery

Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Mutant Stock; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Specieslaboratory mouse
 
Donating Investigator Thomas Doetschman,   University of Arizona

Appearance
white-bellied agouti
Related Genotype: Aw/?

black
Related Genotype: a/a

Description
Mice homozygous for the Tgfb2tm1Doe targeted mutation exhibit perinatal mortality. Homozygous mutant mice exhibit a wide range of developmental defects including cardiac, lung, craniofacial, limb, spinal column, eye, inner and urogenital defects.

Control Information

  Control
   Wild-type from the colony
 
  Considerations for Choosing Controls

Related Strains

Facebase: models
007664   129S-Efnb1tm1Sor/J
000646   A/J
000647   A/WySnJ
005709   B6.129-Skitm1Cco/J
002619   B6.129-Tgfb3tm1Doe/J
007453   B6.129P2(Cg)-Dhcr7tm1Gst/J
010525   B6.129S-Notch2tm3Grid/J
010616   B6.129S1-Jag1tm1Grid/J
010546   B6.129S1-Jag2tm1Grid/J
010620   B6.129S1-Notch2tm1Grid/J
009387   B6.129S1-Osr1tm1Jian/J
009386   B6.129S1-Osr2tm1Jian/J
010621   B6.129S1-Snai1tm2.1Grid/J
010617   B6.129S1-Snai2tm1Grid/J
003865   B6.129S2-Itgavtm1Hyn/J
003755   B6.129S4-Meox2tm1(cre)Sor/J
016902   B6.129S5-Irf6Gt(OST398253)Lex/J
003336   B6.129S7-Cdkn1ctm1Sje/J
012843   B6.129X1(Cg)-Slc32a1tm1.1Bgc/J
000026   B6.C3-Gli3Xt-J/J
004275   B6.Cg-Fignfi/Frk
012844   B6.Cg-Gad1tm1.1Bgc/J
006382   B6;129-Casktm1Sud/J
002711   B6;129-Gabrb3tm1Geh/J
004293   B6;129-Shhtm2Amc/J
012603   B6;129-Tgfbr2tm1Karl/J
010618   B6;129S-Jag1tm2Grid/J
010686   B6;129S-Snai1tm2Grid/J
009389   B6;129S1-Bambitm1Jian/J
010619   B6;129S1-Lfngtm1Grid/J
010547   B6;129S1-Notch3tm1Grid/J
010544   B6;129S1-Notch4tm1Grid/J
010722   B6;129S1-Snai2tm2Grid/J
012463   B6;129S4-Foxd1tm1(GFP/cre)Amc/J
003277   B6;129S7-Acvr2atm1Zuk/J
002788   B6;129S7-Fsttm1Zuk/J
002990   B6;129S7-Inhbatm1Zuk/J
000523   B6By.Cg-Eh/J
000278   B6C3Fe a/a-Papss2bm Hps1ep Hps6ru/J
000515   B6CBACa Aw-J/A-SfnEr/J
001434   C3HeB/FeJ x STX/Le-Mc1rE-so Gli3Xt-J Zeb1Tw/J
000252   DC/LeJ
005057   FVB.129-Kcnj2tm1Swz/J
012655   FVB.A-Irf6clft1/BeiJ
013100   FVB.C-Prdm16csp1/J
017437   FVB/N-Ckap5TgTn(sb-cHS4,Tyr)2320F-1Ove/J
017438   FVB/N-MidnTg(Tyr)2261EOve/J
017609   FVB/N-Rr16Tn(sb-Tyr)1HCebOve/J
017598   FVB/N-Sdccag8Tn(sb-Tyr)2161B.CA1C2Ove/J
017608   FVB/N-Skor2Tn(sb-Tyr)1799B.CA7BOve/J
017436   FVB/N-Tapt1TgTn(sb-cHS4,Tyr)2508GOve/J
016870   FVB/NJ-Ap2b1Tg(Tyr)427Ove/EtevJ
017434   FVB;B6-Cramp1lTgTn(sb-rtTA,Tyr)2447AOve/J
017594   FVB;B6-Eya4TgTn(Prm1-sb10,sb-Tyr)1739AOve/J
017435   FVB;B6-SlmapTn(sb-rtTA)2426B.SB4Ove/J
003318   STOCK Shhtm1Amc/J
018624   STOCK Tgfb3tm2(Tgfb1)Vk/J
008469   STOCK Wnt9btm1.2Amc/J
View Facebase: models     (58 strains)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).
Peters Anomaly
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Loeys-Dietz Syndrome, Type 4; LDS4   (TGFB2)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Tgfb2tm1Doe/Tgfb2+

        involves: 129P2/OlaHsd * Black Swiss
  • endocrine/exocrine gland phenotype
  • abnormal bulbourethral gland morphology
    • adult male heterozygotes exhibit Cowper's gland hyperplasia, local atrophy, ductal transformation and cystic dilation   (MGI Ref ID J:78547)
    • bulbourethral gland hyperplasia
      • adult male heterozygotes exhibit glandular hyperplasia of Cowper's gland with thickening of the surrounding muscular capsule   (MGI Ref ID J:78547)
      • the hyperplastic glandular epithelium is multilayered with large foamy or vacuolated cells and irregular nuclear structure and position   (MGI Ref ID J:78547)
      • hyperplastic Cowper's glands exhibit an ~80% reduction in apoptotic cell death relative to wild-type glands   (MGI Ref ID J:78547)
    • cystic bulbourethral gland
      • heterozygores are viable and fertile; however, some male heterozygotes develop palpable cysts in the perineal/scrotal region (9 cysts in 21 males; 1-2 cysts per animal)   (MGI Ref ID J:78547)
      • young (2-4-mo-old) males have small, externally non-visible cysts   (MGI Ref ID J:78547)
      • older (>7-mo-old) males exhibit large, fluid-filled cysts located deep to the pelvic floor, dorso-laterally of the ischiocavernosus and bulbocavernosus muscles (Cowper's syringoceles), suggesting impaired epithelial-stromal interactions   (MGI Ref ID J:78547)
      • the cellular lining of the cyst wall exhibits heterogeneity of the epithelial lining ranging from single layered squamous epithelium to multilayered glandular structures covering papillary folds   (MGI Ref ID J:78547)
      • severely hyperplastic cells from the cyst wall exhibit extreme overload of polymorphic secretory material; stratified epithelium from the cyst wall is devoid of any signs of secretion   (MGI Ref ID J:78547)
  • prostate gland anterior lobe hyperplasia
    • male heterozygotes exhibit coagulating gland hyperplasia   (MGI Ref ID J:78547)
  • reproductive system phenotype
  • abnormal bulbourethral gland morphology
    • adult male heterozygotes exhibit Cowper's gland hyperplasia, local atrophy, ductal transformation and cystic dilation   (MGI Ref ID J:78547)
    • bulbourethral gland hyperplasia
      • adult male heterozygotes exhibit glandular hyperplasia of Cowper's gland with thickening of the surrounding muscular capsule   (MGI Ref ID J:78547)
      • the hyperplastic glandular epithelium is multilayered with large foamy or vacuolated cells and irregular nuclear structure and position   (MGI Ref ID J:78547)
      • hyperplastic Cowper's glands exhibit an ~80% reduction in apoptotic cell death relative to wild-type glands   (MGI Ref ID J:78547)
    • cystic bulbourethral gland
      • heterozygores are viable and fertile; however, some male heterozygotes develop palpable cysts in the perineal/scrotal region (9 cysts in 21 males; 1-2 cysts per animal)   (MGI Ref ID J:78547)
      • young (2-4-mo-old) males have small, externally non-visible cysts   (MGI Ref ID J:78547)
      • older (>7-mo-old) males exhibit large, fluid-filled cysts located deep to the pelvic floor, dorso-laterally of the ischiocavernosus and bulbocavernosus muscles (Cowper's syringoceles), suggesting impaired epithelial-stromal interactions   (MGI Ref ID J:78547)
      • the cellular lining of the cyst wall exhibits heterogeneity of the epithelial lining ranging from single layered squamous epithelium to multilayered glandular structures covering papillary folds   (MGI Ref ID J:78547)
      • severely hyperplastic cells from the cyst wall exhibit extreme overload of polymorphic secretory material; stratified epithelium from the cyst wall is devoid of any signs of secretion   (MGI Ref ID J:78547)
  • abnormal spermatogenesis
    • male heterozygotes show a reduced yield of spermatogenesis   (MGI Ref ID J:78547)
    • oligozoospermia   (MGI Ref ID J:78547)
    • teratozoospermia
      • male heterozygotes display malformed spermatozoa   (MGI Ref ID J:78547)
  • prostate gland anterior lobe hyperplasia
    • male heterozygotes exhibit coagulating gland hyperplasia   (MGI Ref ID J:78547)

Tgfb2tm1Doe/Tgfb2tm1Doe

        involves: 129P2/OlaHsd * Black Swiss
  • mortality/aging
  • complete neonatal lethality
    • live-born homozygotes respond to mechanical stimulation but generally die within minutes with respiratory distress   (MGI Ref ID J:41682)
    • homozygotes fail to survive beyond 2 hrs due to impaired cardiovascular function   (MGI Ref ID J:73681)
  • partial perinatal lethality
    • two-thirds of homozygotes die shortly before or during birth and the remaining are born cyanotic   (MGI Ref ID J:41682)
  • cardiovascular system phenotype
  • abnormal aorta morphology
    • overall, 33.3% of homozygotes aged E13.5 to 18.5 display structural abnormalities of the aorta or its branches   (MGI Ref ID J:103391)
    • at E11.5-E16.5, increased apoptosis is noted in aortic segments deriving from the fourth arch   (MGI Ref ID J:103391)
    • aberrant origin of the right subclavian artery
      • 2 of 24 (8.3%) of homozygotes display an aberrant right subclavian artery   (MGI Ref ID J:103391)
    • aortic arch hypoplasia
      • 5 of 24 (20.8%) of homozygotes exhibit hypoplasia of the aortic arch and/or ascending aorta   (MGI Ref ID J:103391)
    • ascending aorta hypoplasia
      • at E18.5, homozygotes exhibit a small, thin-walled, hypoplastic ascending aorta   (MGI Ref ID J:41682)
      • 5 of 24 (20.8%) of homozygotes exhibit hypoplasia of the aortic arch and/or ascending aorta   (MGI Ref ID J:103391)
    • interrupted aortic arch
      • 2 of 24 (8.3%) of homozygotes exhibit interruption of the aortic arch   (MGI Ref ID J:103391)
      • 1 of 24 (4.2%) of homozygotes with a common arterial trunk display interruption of the aortic arch type B   (MGI Ref ID J:103391)
  • abnormal atrioventricular valve morphology
    • 8 of 24 (33.3%) of homozygotes display AV valve thickening   (MGI Ref ID J:103391)
    • at E18.5, both tricuspid and mitral valve are abnormally connected to the left ventricle   (MGI Ref ID J:41682)
    • thick mitral valve
      • 3 of 24 (12.5%) of homozygotes with tricuspid valve thickening show additional thickening of the mitral valve   (MGI Ref ID J:103391)
    • thick tricuspid valve
      • 8 of 24 (33.3%) of homozygotes display thickening of tricuspid valve thickening, with additional thickening of the mitral valve in 3 cases   (MGI Ref ID J:103391)
  • abnormal cardiovascular development
    • overall, 87.5% (21 of 24) homozygous mutant embryos aged E13.5 to 18.5 display abnormalities of the heart and great vessels   (MGI Ref ID J:103391)
    • abnormal atrioventricular cushion morphology
      • at E13.5, homozygotes exhibit a normal endocardial cushion volume; however, the normal decrease in total endocardial cushion volume observed in older (E15.5) wild-type embryos does not occur   (MGI Ref ID J:103391)
      • failure of atrioventricular cushion closure
        • in some cases, fusion of the proximal cushions is incomplete   (MGI Ref ID J:103391)
        • incomplete fusion of the endocardial cushions results in a small membranous VSD   (MGI Ref ID J:103391)
        • an extensive perimembranous inlet VSD is seen in cases in which outflow tract and AV cushions do not meet   (MGI Ref ID J:103391)
    • abnormal outflow tract development
      • at E11.5-E16.5, homozygotes display increased apoptosis in the outflow tract relative to wild-type embryos; apoptosis occurs 1 day later (E14.5), and decreases more slowly than normal   (MGI Ref ID J:103391)
      • abnormal truncus arteriosus septation
        • 1 of 24 (4.2%) of homozygotes display a common arterial trunk with interruption of the aortic arch type B   (MGI Ref ID J:103391)
    • failure of heart looping
      • homozygotes display various degrees of failure of normal remodeling of the primitive heart e.g. overriding tricuspid valve and DORV interfering with final phase of cardiac looping and wedging   (MGI Ref ID J:103391)
    • persistent right dorsal aorta
      • 1 of 24 (4.2%) of homozygotes display a remnant of the right dorsal aorta   (MGI Ref ID J:103391)
  • abnormal heart septum morphology
    • at E13.5 to E18.5, homozygotes show a variable degree of hypoplasia of tissues deriving from the outflow tract ridges and the septal parts of the AV cushions   (MGI Ref ID J:103391)
    • atrioventricular septal defect
      • overall, 62.5% (15 of 24) of homozygotes aged E13.5 to 18.5 display defects related to the region of the AV canal and the ventricular inlet segment   (MGI Ref ID J:103391)
      • complete atrioventricular septal defect
        • 1 of 24 (4.2%) of homozygotes display a complete atrioventricular septal defect   (MGI Ref ID J:103391)
    • inlet ventricular septal defect
      • 9 of 24 (37.5%) of homozygotes aged E13.5 to E18.5 show a perimembranous inlet VSD associated with overriding of the tricuspid orifice in 6 cases   (MGI Ref ID J:103391)
      • VSD is more closely related to the aortic orifice in cases with a posterior position of the latter   (MGI Ref ID J:103391)
      • in case of a deficient outflow tract septum, the VSD is committed to both arterial orifices   (MGI Ref ID J:103391)
      • at E18.5, 15 of 16 homozygotes show ventricular septum defects   (MGI Ref ID J:41682)
    • ostium primum atrial septal defect
      • at E18.5, 1 of 24 (4.2%) of homozygotes display a large primum-type of atrial septal defect; the lower rim of atrial septum is still mesenchymal and has not fused with AV cushions   (MGI Ref ID J:103391)
    • perimembraneous ventricular septal defect
      • 6 of 24 (25%) of homozygotes display overriding of tricuspid orifice via a perimembranous inlet VSD   (MGI Ref ID J:103391)
  • abnormal heart ventricle outflow tract morphology
    • dextroposition of the outflow tract results in a large-outlet VSD due to aberrant position of the outflow tract septum relative to the ventricular septum   (MGI Ref ID J:103391)
    • patent aortic valve   (MGI Ref ID J:41682)
    • patent pulmonary valve   (MGI Ref ID J:41682)
    • thick aortic valve cusps
      • 1 of 24 (4.2%) of homozygotes show thickening of the aortic valve leaflets   (MGI Ref ID J:103391)
    • thick pulmonary valve cusps
      • 2 of 24 (8.3%) of homozygotes show thickening of the leaflets of the pulmonary valve, with thickening of the aortic valve in one case   (MGI Ref ID J:103391)
  • abnormal myocardium layer morphology
    • at E18.5, some homozygotes display normal myocardialization of outflow tract cushions; others exhibit absence of myocardialization, with only a small fibrous ridge below the semilunar valves   (MGI Ref ID J:103391)
    • at E18.5, the mutant myocardium is hypercellular and less trabeculated   (MGI Ref ID J:41682)
    • trabecula carnea hypoplasia   (MGI Ref ID J:41682)
  • abnormal semilunar valve morphology
    • 1 of 24 (4.2%) of homozygotes show thickening of the semilunar valve leaflets   (MGI Ref ID J:103391)
    • at E18.5, the aortic and pulmonary orifices are both above the right ventricle; both exhibit valve leaflets that are patent   (MGI Ref ID J:41682)
    • patent aortic valve   (MGI Ref ID J:41682)
    • patent pulmonary valve   (MGI Ref ID J:41682)
    • thick aortic valve cusps
      • 1 of 24 (4.2%) of homozygotes show thickening of the aortic valve leaflets   (MGI Ref ID J:103391)
    • thick pulmonary valve cusps
      • 2 of 24 (8.3%) of homozygotes show thickening of the leaflets of the pulmonary valve, with thickening of the aortic valve in one case   (MGI Ref ID J:103391)
  • dilated heart right ventricle
    • at E15.5, the myocardium of the right ventricle appears spongier, probably due to ventricular dilatation   (MGI Ref ID J:103391)
    • at E18.5, homozygotes exhibit an enlarged right ventricle   (MGI Ref ID J:41682)
  • double inlet heart left ventricle
    • at E18.5, 4 of 16 homozygotes exhibit DILV   (MGI Ref ID J:41682)
  • double outlet right ventricle
    • 79.2% (19 of 24) of homozygotes exhibit a DORV with different relative positions of the arterial orifices, i.e. posterior (13 of 19), side-by-side (3 of 19), or slightly anterior (3 of 19) to the pulmonary orifice   (MGI Ref ID J:103391)
    • all mutant hearts with DORV display a bilateral muscular conus   (MGI Ref ID J:103391)
    • at E18.5, 3 of 16 homozygotes exhibit DORV   (MGI Ref ID J:41682)
  • heart valve hyperplasia
    • in contrast to septal hypoplasia, E18.5 homozygotes show abnormalities of AV and semilunar valve differentiation   (MGI Ref ID J:103391)
    • mutant valve leaflets are hyperplastic and retain a thick and cushion-like appearance   (MGI Ref ID J:103391)
    • right-sided valves (tricuspid and pulmonary) are more frequently affected than left-sided valves (mitral and aortic)   (MGI Ref ID J:103391)
  • pulmonary artery hypoplasia
    • 1 of 24 (4.2%) of homozygotes display a hypoplastic pulmonary artery   (MGI Ref ID J:103391)
  • hearing/vestibular/ear phenotype
  • abnormal cochlea morphology   (MGI Ref ID J:41682)
    • abnormal scala vestibuli morphology
      • at E18.5, all homozygotes show incomplete canalization of the scala vestibuli   (MGI Ref ID J:41682)
      • a wider space between the epithelial ridge and basilar membrane is observed   (MGI Ref ID J:41682)
    • absent Rosenthal canal   (MGI Ref ID J:41682)
    • absent interdental cells
      • the interdental cells overlying the spiral limbus appear undifferentiated   (MGI Ref ID J:41682)
    • absent spiral limbus
      • unlike wild-type mice, all homozygotes fail to form the spiral limbus in the basal cochlear turn by E18.5   (MGI Ref ID J:41682)
  • homeostasis/metabolism phenotype
  • cyanosis
    • one-third of homozygotes that are born live exhibit congenital cyanosis   (MGI Ref ID J:41682)
  • increased urine protein level   (MGI Ref ID J:41682)
  • endocrine/exocrine gland phenotype
  • ectopic adrenal gland
    • at E18.5, 1 of 5 female homozygotes shows adrenal ectopia   (MGI Ref ID J:41682)
  • ectopic testis
    • at E18.5, all male homozygotes exhibit testicular ectopia   (MGI Ref ID J:41682)
  • testis hypoplasia
    • at E18.5, 1 of 5 males displays unilateral testicular hypoplasia with absence of an epididymis and vas deferens dysgenesis   (MGI Ref ID J:41682)
  • immune system phenotype
  • abnormal macrophage physiology
    • at E13.5 or later, homozygotes exhibit failure of macrophage invasion into ocular tissues, suggesting impaired removal of vitreous hyaline cells   (MGI Ref ID J:73681)
  • reproductive system phenotype
  • abnormal uterine horn morphology
    • at E18.5, 2 of 5 female homozygotes display uterine horn ectopia by ventral displacement relative to the kidneys   (MGI Ref ID J:41682)
  • ectopic testis
    • at E18.5, all male homozygotes exhibit testicular ectopia   (MGI Ref ID J:41682)
  • testis hypoplasia
    • at E18.5, 1 of 5 males displays unilateral testicular hypoplasia with absence of an epididymis and vas deferens dysgenesis   (MGI Ref ID J:41682)
  • respiratory system phenotype
  • atelectasis
    • postnatally, all mutant lungs display collapsed terminal and respiratory bronchioles   (MGI Ref ID J:41682)
  • dilated respiratory conducting tubes
    • postnatally, all mutant lungs exhibit dilated conducting airways   (MGI Ref ID J:41682)
  • respiratory distress
    • live-born homozygotes exhibit respiratory distress   (MGI Ref ID J:41682)
  • skeleton phenotype
  • abnormal clavicle morphology
    • at E18.5, homozygotes show ventral curvature of the clavicles   (MGI Ref ID J:41682)
  • abnormal craniofacial bone morphology
    • at E18.5, all homozygotes exhibit reduced cranial ossification of the frontal, interparietal, parietal and squamosal bones   (MGI Ref ID J:41682)
    • abnormal mandible morphology
      • at E18.5, the masseteric ridge is more prominent and anteriorly and dorsally displaced   (MGI Ref ID J:41682)
      • abnormal mandibular condyloid process morphology
        • at E18.5, the condyloid process is reduced to one-half of wild-type size   (MGI Ref ID J:41682)
      • abnormal mandibular coronoid process morphology
        • at E18.5, the coronoid process is reduced to one-half of wild-type size   (MGI Ref ID J:41682)
      • absent mandibular angle
        • at E18.5, all mutant mandibles lack an angle   (MGI Ref ID J:41682)
      • short mandible   (MGI Ref ID J:41682)
    • abnormal neurocranium morphology
      • at E18.5, most homozygotes display dysmorphic calvaria   (MGI Ref ID J:41682)
      • absent alisphenoid bone
        • at E18.5, all homozygotes show a nearly complete agenesis of the alisphenoid bone   (MGI Ref ID J:41682)
      • absent occipital bone
        • at E18.5, all homozygotes show a nearly complete agenesis of the occipital bone   (MGI Ref ID J:41682)
      • absent pterygoid process
        • at E18.5, homozygotes with cleft palate (23%) show absence of the pterygoid process of the basisphenoid bone   (MGI Ref ID J:41682)
      • large anterior fontanelle
        • at E18.5, all homozygotes display enlarged fontanelles   (MGI Ref ID J:41682)
      • small frontal bone
        • at E18.5, all homozygotes exhibit reduced frontal bones   (MGI Ref ID J:41682)
      • small interparietal bone
        • at E18.5, all homozygotes exhibit reduced interparietal bones   (MGI Ref ID J:41682)
      • small parietal bone
        • at E18.5, all homozygotes exhibit reduced parietal bones   (MGI Ref ID J:41682)
      • small temporal bone
        • at E18.5, all homozygotes exhibit reduced temporal bones   (MGI Ref ID J:41682)
    • absent maxillary shelf
      • at E18.5, homozygotes with cleft palate (23%) show absence of the palatine shelf   (MGI Ref ID J:41682)
    • retrognathia
      • at E18.5, most homozygotes display retrognathia   (MGI Ref ID J:41682)
  • abnormal femur morphology   (MGI Ref ID J:41682)
    • abnormal trochanter morphology
      • all newborn homozygotes lack the third trochanter on the femur   (MGI Ref ID J:41682)
  • abnormal humerus morphology   (MGI Ref ID J:41682)
    • absent deltoid tuberosity
      • all newborn homozygotes lack the deltoid tuberosity on the humerus   (MGI Ref ID J:41682)
  • abnormal rib morphology
    • one-third of homozygotes exhibit wavy irregular ribs or fused ribs   (MGI Ref ID J:41682)
    • rib fusion
      • at E18.5, 2 of 16 homozygotes display rib fusions   (MGI Ref ID J:41682)
  • abnormal sternum morphology
    • at E18.5, 4 of 16 homozygotes display sternum abnormalities, including bifurcation, incomplete manubrium, and vestigial xiphoid process   (MGI Ref ID J:41682)
    • abnormal xiphoid process morphology
      • at E18.5, 4 of 16 homozygotes display a vestigial xiphoid process   (MGI Ref ID J:41682)
  • abnormal thoracic cage shape
    • at E18.5, 15 of 16 homozygotes exhibit rib barreling, resulting in a larger, more rounded pulmonary cavity   (MGI Ref ID J:41682)
  • short radius
    • all newborn homozygotes exhibit a shortened radius   (MGI Ref ID J:41682)
  • short ulna
    • all newborn homozygotes exhibit a shortened ulna with a reduced olecranon process   (MGI Ref ID J:41682)
  • spina bifida occulta
    • newborn homozygotes exhibit spina bifida occulta   (MGI Ref ID J:41682)
    • mutant neural arches form but fail to fuse at the midline of the neural tube   (MGI Ref ID J:41682)
    • typically, neural arch defects range from the 10th thoracic to the 5th caudal vertebra   (MGI Ref ID J:41682)
  • vision/eye phenotype
  • abnormal corneal stroma morphology
    • at E14.5-E18.5, the central stroma adheres to the lens capsule   (MGI Ref ID J:73681)
    • at E18.5, reduced collagenous matrix accumulation is noted in the extracellular space between stromal keratocytes   (MGI Ref ID J:73681)
    • abnormal posterior stroma morphology
      • at E18.5, cells at the posterior stroma fail to form a continuous endothelial cell layer   (MGI Ref ID J:73681)
      • no intercellular junctional complex or basal lamella-like structure is observed in the posterior cornea   (MGI Ref ID J:73681)
    • decreased corneal stroma thickness
      • at E18.5, all homozygotes display reduced corneal stroma thickness (~33% of wild-type)   (MGI Ref ID J:41682)
      • at E13.5-E14.5, the mutant corneal stroma is significantly thinner with fewer keratocytes than wild-type stroma   (MGI Ref ID J:73681)
      • intercellular spacing is reduced due to decreased ECM accumulation (collagen I, lumican, and keratocan) rather than impaired keratocyte proliferation or enhanced keratocyte apoptosis   (MGI Ref ID J:73681)
  • abnormal eye anterior chamber morphology
    • at E14.5, an anterior chamber fails to form   (MGI Ref ID J:73681)
  • abnormal eye posterior chamber morphology
    • at E18.5, all homozygotes contain a hypercellular infusion of vascularized melanocytes, neuronal cells, and mesenchymal cells in the posterior eye chamber   (MGI Ref ID J:41682)
  • abnormal iris stroma morphology
    • at E18.5, the mutant iris stroma is underdeveloped   (MGI Ref ID J:73681)
  • abnormal retinal neuronal layer morphology
    • the mutant neural retina fails to laminate and undergo normal differentiation by E18.5   (MGI Ref ID J:73681)
  • absent Descemet membrane
    • at E14.5, a Descemet's membrane fails to form   (MGI Ref ID J:73681)
  • absent corneal endothelium
    • at E14.5, no endothelium forms in cornea, limbus and trabecular meshworks   (MGI Ref ID J:73681)
    • in contrast, corneal epithelium morphology appears unaffected   (MGI Ref ID J:73681)
  • decreased cornea thickness
    • at E13.5-E14.5, the mutant cornea is abnormally thin   (MGI Ref ID J:73681)
    • decreased corneal stroma thickness
      • at E18.5, all homozygotes display reduced corneal stroma thickness (~33% of wild-type)   (MGI Ref ID J:41682)
      • at E13.5-E14.5, the mutant corneal stroma is significantly thinner with fewer keratocytes than wild-type stroma   (MGI Ref ID J:73681)
      • intercellular spacing is reduced due to decreased ECM accumulation (collagen I, lumican, and keratocan) rather than impaired keratocyte proliferation or enhanced keratocyte apoptosis   (MGI Ref ID J:73681)
  • fused cornea and lens
    • at E13.5-E14.5, the mutant cornea fails to separate from the lens   (MGI Ref ID J:73681)
  • persistence of hyaloid vascular system
    • at E18.5, remnant capillaries are found between the stroma and lens capsule   (MGI Ref ID J:73681)
  • retina hyperplasia
    • at E18.5, all homozygotes show hyperplasia of both the inner and outer neuroblastic layers of the retina   (MGI Ref ID J:41682)
  • vitreous body deposition
    • at E18.5, a huge cell mass of hyalocytes and blood cells accumulates in the vitreous   (MGI Ref ID J:73681)
  • nervous system phenotype
  • abnormal cochlear ganglion morphology
    • at E18.5, the mutant spiral ganglion abnormally lies close to the sensory epithelium due to absence of the spiral limbus and Rosenthal's canal   (MGI Ref ID J:41682)
  • spina bifida occulta
    • newborn homozygotes exhibit spina bifida occulta   (MGI Ref ID J:41682)
    • mutant neural arches form but fail to fuse at the midline of the neural tube   (MGI Ref ID J:41682)
    • typically, neural arch defects range from the 10th thoracic to the 5th caudal vertebra   (MGI Ref ID J:41682)
  • muscle phenotype
  • trabecula carnea hypoplasia   (MGI Ref ID J:41682)
  • limbs/digits/tail phenotype
  • abnormal limb morphology
    • newborn homozygotes display limb laxity; both fore- and hindlimbs are rotated and extend toward the midline   (MGI Ref ID J:41682)
    • abnormal femur morphology   (MGI Ref ID J:41682)
      • abnormal trochanter morphology
        • all newborn homozygotes lack the third trochanter on the femur   (MGI Ref ID J:41682)
    • abnormal humerus morphology   (MGI Ref ID J:41682)
      • absent deltoid tuberosity
        • all newborn homozygotes lack the deltoid tuberosity on the humerus   (MGI Ref ID J:41682)
    • short radius
      • all newborn homozygotes exhibit a shortened radius   (MGI Ref ID J:41682)
    • short ulna
      • all newborn homozygotes exhibit a shortened ulna with a reduced olecranon process   (MGI Ref ID J:41682)
  • growth/size phenotype
  • decreased body weight
    • E18.5 homozygotes delivered by Cesarean section show a 12% reduction in birth weight   (MGI Ref ID J:41682)
  • craniofacial phenotype
  • abnormal craniofacial bone morphology
    • at E18.5, all homozygotes exhibit reduced cranial ossification of the frontal, interparietal, parietal and squamosal bones   (MGI Ref ID J:41682)
    • abnormal mandible morphology
      • at E18.5, the masseteric ridge is more prominent and anteriorly and dorsally displaced   (MGI Ref ID J:41682)
      • abnormal mandibular condyloid process morphology
        • at E18.5, the condyloid process is reduced to one-half of wild-type size   (MGI Ref ID J:41682)
      • abnormal mandibular coronoid process morphology
        • at E18.5, the coronoid process is reduced to one-half of wild-type size   (MGI Ref ID J:41682)
      • absent mandibular angle
        • at E18.5, all mutant mandibles lack an angle   (MGI Ref ID J:41682)
      • short mandible   (MGI Ref ID J:41682)
    • abnormal neurocranium morphology
      • at E18.5, most homozygotes display dysmorphic calvaria   (MGI Ref ID J:41682)
      • absent alisphenoid bone
        • at E18.5, all homozygotes show a nearly complete agenesis of the alisphenoid bone   (MGI Ref ID J:41682)
      • absent occipital bone
        • at E18.5, all homozygotes show a nearly complete agenesis of the occipital bone   (MGI Ref ID J:41682)
      • absent pterygoid process
        • at E18.5, homozygotes with cleft palate (23%) show absence of the pterygoid process of the basisphenoid bone   (MGI Ref ID J:41682)
      • large anterior fontanelle
        • at E18.5, all homozygotes display enlarged fontanelles   (MGI Ref ID J:41682)
      • small frontal bone
        • at E18.5, all homozygotes exhibit reduced frontal bones   (MGI Ref ID J:41682)
      • small interparietal bone
        • at E18.5, all homozygotes exhibit reduced interparietal bones   (MGI Ref ID J:41682)
      • small parietal bone
        • at E18.5, all homozygotes exhibit reduced parietal bones   (MGI Ref ID J:41682)
      • small temporal bone
        • at E18.5, all homozygotes exhibit reduced temporal bones   (MGI Ref ID J:41682)
    • absent maxillary shelf
      • at E18.5, homozygotes with cleft palate (23%) show absence of the palatine shelf   (MGI Ref ID J:41682)
    • retrognathia
      • at E18.5, most homozygotes display retrognathia   (MGI Ref ID J:41682)
  • cleft secondary palate
    • at E18.5, 23% of homozygotes display an extensive anteroposterior cleft of the secondary palate, leaving the nasal septa exposed and extending into the soft palate   (MGI Ref ID J:41682)
    • no primary palate cleft or cleft lip was ever observed   (MGI Ref ID J:41682)
    • failure of palatal shelf elevation
      • observed at day E18.5, mice show a failure of the palatal shelves to elevate into a horizontal orientation for the process of apposition and fusion   (MGI Ref ID J:41682)
  • renal/urinary system phenotype
  • abnormal kidney morphology
    • following tubulogenesis, female homozygotes show renal dysplastic changes, including renal tubule dilatation, degeneration of the tubular epithelium, proteinuria, and enlargement of the renal pelvis   (MGI Ref ID J:41682)
    • abnormal renal tubule epithelium morphology
      • when kidneys form in females, tubulogenesis is followed by degeneration of the tubular epithelium   (MGI Ref ID J:41682)
    • absent kidney
      • at E18.5, 1 of 5 homozygotes (females only) shows renal agenesis   (MGI Ref ID J:41682)
    • dilated renal tubules
      • when kidneys form in females, tubulogenesis is followed by progressive tubule dilatation   (MGI Ref ID J:41682)
    • hydronephrosis
      • at E18.5, 3 of 10 homozygotes show a dilated renal pelvis   (MGI Ref ID J:41682)
  • increased urine protein level   (MGI Ref ID J:41682)
  • digestive/alimentary phenotype
  • absent maxillary shelf
    • at E18.5, homozygotes with cleft palate (23%) show absence of the palatine shelf   (MGI Ref ID J:41682)
  • cleft secondary palate
    • at E18.5, 23% of homozygotes display an extensive anteroposterior cleft of the secondary palate, leaving the nasal septa exposed and extending into the soft palate   (MGI Ref ID J:41682)
    • no primary palate cleft or cleft lip was ever observed   (MGI Ref ID J:41682)
    • failure of palatal shelf elevation
      • observed at day E18.5, mice show a failure of the palatal shelves to elevate into a horizontal orientation for the process of apposition and fusion   (MGI Ref ID J:41682)
  • embryogenesis phenotype
  • spina bifida occulta
    • newborn homozygotes exhibit spina bifida occulta   (MGI Ref ID J:41682)
    • mutant neural arches form but fail to fuse at the midline of the neural tube   (MGI Ref ID J:41682)
    • typically, neural arch defects range from the 10th thoracic to the 5th caudal vertebra   (MGI Ref ID J:41682)

The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.

Tgfb2tm1Doe/Tgfb2+

        involves: 129/Sv * 129P2/OlaHsd * Black Swiss * C57BL/6J
  • nervous system phenotype
  • decreased dopamine level
    • in aged (6-month old) mice, dopamine levels are only 70% of wild-type levels in the striatum; at 6 months, the dihydroxyphenyacetic acid/dopamine ratio (DOPAC/dopamine) is significantly increased relative to wild-type   (MGI Ref ID J:108007)
  • decreased dopaminergic neuron number
    • heterozygotes have 12% fewer dopaminergic neurons than wild-type littermates at 6 weeks of age; no further reduction is seen at 6 months of age   (MGI Ref ID J:108007)
  • homeostasis/metabolism phenotype
  • decreased dopamine level
    • in aged (6-month old) mice, dopamine levels are only 70% of wild-type levels in the striatum; at 6 months, the dihydroxyphenyacetic acid/dopamine ratio (DOPAC/dopamine) is significantly increased relative to wild-type   (MGI Ref ID J:108007)

Tgfb2tm1Doe/Tgfb2+

        involves: 129P2/OlaHsd
  • digestive/alimentary phenotype
  • abnormal enterocyte apoptosis
    • mice exhibit reduced enterocyte apoptosis in the small intestine compared with wild-type mice   (MGI Ref ID J:76342)
    • however, enterocyte apoptosis in the colon is normal   (MGI Ref ID J:76342)
  • abnormal small intestinal villus morphology
    • villus length is increased compared to in wild-type mice   (MGI Ref ID J:76342)
  • cellular phenotype
  • abnormal enterocyte apoptosis
    • mice exhibit reduced enterocyte apoptosis in the small intestine compared with wild-type mice   (MGI Ref ID J:76342)
    • however, enterocyte apoptosis in the colon is normal   (MGI Ref ID J:76342)

Tgfb2tm1Doe/Tgfb2tm1Doe

        involves: 129P2/OlaHsd * C57BL/6
  • vision/eye phenotype
  • primary vitreous hyperplasia
    • by E13.5 mice display increased cell density in the primary vitreous   (MGI Ref ID J:149526)
    • at E18.5 and P0 mice display primary vitreous hyperplasia   (MGI Ref ID J:149526)

Tgfb2tm1Doe/Tgfb2tm1Doe

        involves: 129P2/OlaHsd
  • limbs/digits/tail phenotype
  • *normal* limbs/digits/tail phenotype
    • mice exhibit normal apoptosis of interdigital webbing   (MGI Ref ID J:76541)
View Research Applications

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

Tgfb2tm1Doe related

Cancer Research
Growth Factors/Receptors/Cytokines

Immunology, Inflammation and Autoimmunity Research
Growth Factors/Receptors/Cytokines

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Tgfb2tm1Doe
Allele Name targeted mutation 1, Thomas Doetschman
Allele Type Targeted (knock-out)
Common Name(s) TGBbeta2-; TGF-beta2-; Tgfb2-;
Mutation Made By Thomas Doetschman,   University of Arizona
Strain of Origin129P2/OlaHsd
ES Cell Line NameE14.1
ES Cell Line Strain129P2/OlaHsd
Gene Symbol and Name Tgfb2, transforming growth factor, beta 2
Chromosome 1
Gene Common Name(s) BB105277; LDS4; TGF-B2; TGF-beta2; Tgfb-2; expressed sequence BB105277;
General Note Homozygotes exhibit a "Peters'-like" anomaly instead of an Axenfeld-Reiger's and Peter's anomaly (J:73681).
Molecular Note Exon 6 was disrupted by the insertion of a neomycin selection cassette. The insertion introduced stop codons in all three reading frames. RT-PCR analysis showed an absence of normal message in homozygous mutant mice. [MGI Ref ID J:41682]

Genotyping

Genotyping Information

Genotyping Protocols

Tgfb2tm1Doe, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Sanford LP; Ormsby I; Gittenberger-de Groot AC; Sariola H; Friedman R; Boivin GP; Cardell EL; Doetschman T. 1997. TGFbeta2 knockout mice have multiple developmental defects that are non-overlapping with other TGFbeta knockout phenotypes. Development 124(13):2659-70. [PubMed: 9217007]  [MGI Ref ID J:41682]

Additional References

Langer JC; Henckaerts E; Orenstein J; Snoeck HW. 2004. Quantitative Trait Analysis Reveals Transforming Growth Factor-{beta}2 as a Positive Regulator of Early Hematopoietic Progenitor and Stem Cell Function. J Exp Med 199(1):5-14. [PubMed: 14707111]  [MGI Ref ID J:87437]

Paradis H; Liu CY; Saika S; Azhar M; Doetschman T; Good WV; Nayak R; Laver N; Kao CW; Kao WW; Gendron RL. 2002. Tubedown-1 in remodeling of the developing vitreal vasculature in vivo and regulation of capillary outgrowth in vitro. Dev Biol 249(1):140-55. [PubMed: 12217325]  [MGI Ref ID J:78769]

Tgfb2tm1Doe related

Andrews ZB; Zhao H; Frugier T; Meguro R; Grattan DR; Koishi K; McLennan IS. 2006. Transforming growth factor beta2 haploinsufficient mice develop age-related nigrostriatal dopamine deficits. Neurobiol Dis 21(3):568-75. [PubMed: 16257223]  [MGI Ref ID J:108007]

Avagyan S; Aguilo F; Kamezaki K; Snoeck HW. 2011. Quantitative trait mapping reveals a regulatory axis involving peroxisome proliferator-activated receptors, PRDM16, transforming growth factor-beta2 and FLT3 in hematopoiesis. Blood 118(23):6078-86. [PubMed: 21967974]  [MGI Ref ID J:179097]

Avagyan S; Glouchkova L; Choi J; Snoeck HW. 2008. A quantitative trait locus on chromosome 4 affects cycling of hematopoietic stem and progenitor cells through regulation of TGF-beta2 responsiveness. J Immunol 181(9):5904-11. [PubMed: 18941179]  [MGI Ref ID J:140749]

Azhar M; Brown K; Gard C; Chen H; Rajan S; Elliott DA; Stevens MV; Camenisch TD; Conway SJ; Doetschman T. 2011. Transforming growth factor Beta2 is required for valve remodeling during heart development. Dev Dyn :. [PubMed: 21780244]  [MGI Ref ID J:174611]

Azhar M; Runyan RB; Gard C; Sanford LP; Miller ML; Andringa A; Pawlowski S; Rajan S; Doetschman T. 2009. Ligand-specific function of transforming growth factor beta in epithelial-mesenchymal transition in heart development. Dev Dyn 238(2):431-42. [PubMed: 19161227]  [MGI Ref ID J:144180]

Bartram U; Molin DG; Wisse LJ; Mohamad A; Sanford LP; Doetschman T; Speer CP; Poelmann RE; Gittenberger-de Groot AC. 2001. Double-outlet right ventricle and overriding tricuspid valve reflect disturbances of looping, myocardialization, endocardial cushion differentiation, and apoptosis in TGF-beta(2)-knockout mice. Circulation 103(22):2745-52. [PubMed: 11390347]  [MGI Ref ID J:103391]

Dunker N; Aumuller G. 2002. Transforming growth factor-beta 2 heterozygous mutant mice exhibit Cowper's gland hyperplasia and cystic dilations of the gland ducts (Cowper's syringoceles). J Anat 201(Pt 2):173-83. [PubMed: 12220125]  [MGI Ref ID J:78547]

Dunker N; Krieglstein K. 2003. Reduced programmed cell death in the retina and defects in lens and cornea of Tgfbeta2(-/-) Tgfbeta3(-/-) double-deficient mice. Cell Tissue Res 313(1):1-10. [PubMed: 12838410]  [MGI Ref ID J:105113]

Dunker N; Schmitt K; Krieglstein K. 2002. TGF-beta is required for programmed cell death in interdigital webs of the developing mouse limb. Mech Dev 113(2):111-20. [PubMed: 11960699]  [MGI Ref ID J:76541]

Dunker N; Schmitt K; Schuster N; Krieglstein K. 2002. The role of transforming growth factor beta-2, beta-3 in mediating apoptosis in the murine intestinal mucosa. Gastroenterology 122(5):1364-75. [PubMed: 11984523]  [MGI Ref ID J:76342]

Foitzik K; Paus R; Doetschman T; Dotto GP. 1999. The TGF-beta2 isoform is both a required and sufficient inducer of murine hair follicle morphogenesis. Dev Biol 212(2):278-89. [PubMed: 10433821]  [MGI Ref ID J:56937]

Freeman-Anderson NE; Zheng Y; McCalla-Martin AC; Treanor LM; Zhao YD; Garfin PM; He TC; Mary MN; Thornton JD; Anderson C; Gibbons M; Saab R; Baumer SH; Cunningham JM; Skapek SX. 2009. Expression of the Arf tumor suppressor gene is controlled by Tgf{beta}2 during development. Development 136(12):2081-9. [PubMed: 19465598]  [MGI Ref ID J:149526]

Heupel K; Sargsyan V; Plomp JJ; Rickmann M; Varoqueaux F; Zhang W; Krieglstein K. 2008. Loss of transforming growth factor-beta 2 leads to impairment of central synapse function. Neural Dev 3:25. [PubMed: 18854036]  [MGI Ref ID J:160737]

Iwao K; Inatani M; Matsumoto Y; Ogata-Iwao M; Takihara Y; Irie F; Yamaguchi Y; Okinami S; Tanihara H. 2009. Heparan sulfate deficiency leads to Peters anomaly in mice by disturbing neural crest TGF-beta2 signaling. J Clin Invest 119(7):1997-2008. [PubMed: 19509472]  [MGI Ref ID J:152572]

Iwata J; Hacia JG; Suzuki A; Sanchez-Lara PA; Urata M; Chai Y. 2012. Modulation of noncanonical TGF-beta signaling prevents cleft palate in Tgfbr2 mutant mice. J Clin Invest 122(3):873-85. [PubMed: 22326956]  [MGI Ref ID J:184481]

Jamora C; Lee P; Kocieniewski P; Azhar M; Hosokawa R; Chai Y; Fuchs E. 2005. A signaling pathway involving TGF-beta2 and snail in hair follicle morphogenesis. PLoS Biol 3(1):e11. [PubMed: 15630473]  [MGI Ref ID J:97750]

Kubalak SW; Hutson DR; Scott KK; Shannon RA. 2002. Elevated transforming growth factor beta2 enhances apoptosis and contributes to abnormal outflow tract and aortic sac development in retinoic X receptor alpha knockout embryos. Development 129(3):733-46. [PubMed: 11830573]  [MGI Ref ID J:74237]

Kumar R; Langer JC; Snoeck HW. 2006. Transforming growth factor-beta2 is involved in quantitative genetic variation in thymic involution. Blood 107(5):1974-9. [PubMed: 16282338]  [MGI Ref ID J:129377]

Langer JC; Henckaerts E; Orenstein J; Snoeck HW. 2004. Quantitative Trait Analysis Reveals Transforming Growth Factor-{beta}2 as a Positive Regulator of Early Hematopoietic Progenitor and Stem Cell Function. J Exp Med 199(1):5-14. [PubMed: 14707111]  [MGI Ref ID J:87437]

Letterio JJ; Bottinger EP. 1998. TGF-beta knockout and dominant-negative receptor transgenic mice. Miner Electrolyte Metab 24(2-3):161-7. [PubMed: 9525700]  [MGI Ref ID J:46776]

Li P; Pashmforoush M; Sucov HM. 2010. Retinoic acid regulates differentiation of the secondary heart field and TGFbeta-mediated outflow tract septation. Dev Cell 18(3):480-5. [PubMed: 20230754]  [MGI Ref ID J:159110]

Lindsay ME; Schepers D; Bolar NA; Doyle JJ; Gallo E; Fert-Bober J; Kempers MJ; Fishman EK; Chen Y; Myers L; Bjeda D; Oswald G; Elias AF; Levy HP; Anderlid BM; Yang MH; Bongers EM; Timmermans J; Braverman AC; Canham N; Mortier GR; Brunner HG; Byers PH; Van Eyk J; Van Laer L; Dietz HC; Loeys BL. 2012. Loss-of-function mutations in TGFB2 cause a syndromic presentation of thoracic aortic aneurysm. Nat Genet 44(8):922-7. [PubMed: 22772368]  [MGI Ref ID J:188799]

Memon MA; Anway MD; Covert TR; Uzumcu M; Skinner MK. 2008. Transforming growth factor beta (TGFbeta1, TGFbeta2 and TGFbeta3) null-mutant phenotypes in embryonic gonadal development. Mol Cell Endocrinol 294(1-2):70-80. [PubMed: 18790002]  [MGI Ref ID J:145458]

Molin DG; DeRuiter MC; Wisse LJ; Azhar M; Doetschman T; Poelmann RE; Gittenberger-de Groot AC. 2002. Altered apoptosis pattern during pharyngeal arch artery remodelling is associated with aortic arch malformations in Tgfbeta2 knock-out mice. Cardiovasc Res 56(2):312-22. [PubMed: 12393102]  [MGI Ref ID J:102822]

Molin DG; Poelmann RE; DeRuiter MC; Azhar M; Doetschman T; Gittenberger-de Groot AC. 2004. Transforming growth factor beta-SMAD2 signaling regulates aortic arch innervation and development. Circ Res 95(11):1109-17. [PubMed: 15528466]  [MGI Ref ID J:95075]

Nakazaki H; Shen YW; Yun B; Reddy A; Khanna V; Mania-Farnell BM; Ichi S; Mclone DG Tomita T; Mayanil SK. 2009. Transcriptional regulation by Pax3 and TGFbeta2 signaling: a potential gene regulatory network in neural crest development Int J Biol 53:69-70.  [MGI Ref ID J:142494]

Pangas SA. 2012. Regulation of the ovarian reserve by members of the transforming growth factor beta family. Mol Reprod Dev 79(10):666-79. [PubMed: 22847922]  [MGI Ref ID J:190579]

Paradies NE; Sanford LP; Doetschman T; Friedman RA. 1998. Developmental expression of the TGF beta s in the mouse cochlea. Mech Dev 79(1-2):165-8. [PubMed: 10349630]  [MGI Ref ID J:52221]

Paradis H; Liu CY; Saika S; Azhar M; Doetschman T; Good WV; Nayak R; Laver N; Kao CW; Kao WW; Gendron RL. 2002. Tubedown-1 in remodeling of the developing vitreal vasculature in vivo and regulation of capillary outgrowth in vitro. Dev Biol 249(1):140-55. [PubMed: 12217325]  [MGI Ref ID J:78769]

Poelmann RE; Jongbloed MR; Molin DG; Fekkes ML; Wang Z; Fishman GI; Doetschman T; Azhar M; Gittenberger-de Groot AC. 2004. The neural crest is contiguous with the cardiac conduction system in the mouse embryo: a role in induction? Anat Embryol (Berl) 208(5):389-93. [PubMed: 15248063]  [MGI Ref ID J:154017]

Pryce BA; Watson SS; Murchison ND; Staverosky JA; Dunker N; Schweitzer R. 2009. Recruitment and maintenance of tendon progenitors by TGF{beta} signaling are essential for tendon formation. Development 136(8):1351-61. [PubMed: 19304887]  [MGI Ref ID J:147280]

Roussa E; Wiehle M; Dunker N; Becker-Katins S; Oehlke O; Krieglstein K. 2006. Transforming growth factor beta is required for differentiation of mouse mesencephalic progenitors into dopaminergic neurons in vitro and in vivo: ectopic induction in dorsal mesencephalon. Stem Cells 24(9):2120-9. [PubMed: 16741229]  [MGI Ref ID J:174490]

Saika S; Saika S; Liu CY; Azhar M; Sanford LP; Doetschman T; Gendron RL; Kao CW; Kao WW. 2001. TGFbeta2 in corneal morphogenesis during mouse embryonic development. Dev Biol 240(2):419-32. [PubMed: 11784073]  [MGI Ref ID J:73681]

Short K; Hodson M; Smyth I. 2013. Spatial mapping and quantification of developmental branching morphogenesis. Development 140(2):471-8. [PubMed: 23193168]  [MGI Ref ID J:191063]

Short KM; Hodson MJ; Smyth IM. 2010. Tomographic quantification of branching morphogenesis and renal development. Kidney Int 77(12):1132-9. [PubMed: 20200502]  [MGI Ref ID J:184274]

Vogel T; Ahrens S; Buttner N; Krieglstein K. 2010. Transforming growth factor beta promotes neuronal cell fate of mouse cortical and hippocampal progenitors in vitro and in vivo: identification of Nedd9 as an essential signaling component. Cereb Cortex 20(3):661-71. [PubMed: 19587023]  [MGI Ref ID J:174166]

Walker KA; Cai X; Caruana G; Thomas MC; Bertram JF; Kett MM. 2012. High nephron endowment protects against salt-induced hypertension. Am J Physiol Renal Physiol 303(2):F253-8. [PubMed: 22573381]  [MGI Ref ID J:187017]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

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

Colony Maintenance

Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $1980.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.
    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 11 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory 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. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2574.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.
    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 11 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory 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. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

General Supply Notes

Control Information

  Control
   Wild-type from the colony
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.


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The Jackson Laboratory's Genotype Promise

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.
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JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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