Strain Name:

129S/Sv-Rettm1Cos/J

Stock Number:

009085

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Availability:

Cryopreserved - Ready for recovery

Use Restrictions Apply, see Terms of Use
Mice homozygous for the Ret- allele harbor a knockout of the ret proto-oncogene locus and may be useful in studying kidney/urinary and peripheral nervous system development, as well as abnormal enteric neural crest cell migration and Hirschsprung's Disease.

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 Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Specieslaboratory mouse
Generation?pN1
Generation Definitions
 
Donating Investigator Frank Costantini,   Columbia University Medical Center

Description
The Ret- allele (also called ret-k-, ret-k minus, or c-ret-) disrupts the region of the ret proto-oncogene (Ret; also called ret-k or c-ret) locus harboring the invariant lysine codon required for Ret kinase activity. Homozygous mice die around 16-24 hours after birth, exhibiting abnormalities in kidney/urinary (renal agenesis/hypodysplasia) and peripheral nervous system development (including sympathetic, parasympathetic, and enteric ganglia), as well as abnormal enteric neural crest cell migration. Because homozygous mice lack enteric ganglia from the hindgut, these mice are also a model of Hirschsprung's Disease.

Development
A targeting vector was designed to replace an 0.8 kb region of the ret proto-oncogene (Ret; also called ret-k or c-ret) locus, including the codon for an invariant lysine required for Ret kinase activity, with a neomycin resistance cassette. The construct was electroporated into 129S/SvEv-Gpi1c derived CCE embryonic stem (ES) cells. Correctly targeted ES cells were injected into recipient blastocysts and chimeric mice were bred with 129/SvEv mice to establish the colony. Heterozygous mice were bred with wildtype 129/SvEv (and/or 129S6/SvEvTac) mice for many generations prior to sending to The Jackson Laboratory Repository. Upon arrival, mice were bred together 129S1/SvImJ inbred mice (Stock No. 002448) for at least one generation to establish the colony.

Control Information

  Control
   Wild-type from the colony
   002448 129S1/SvImJ
 
  Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Ret
016234   B6.129S1(FVB)-Rettm2.1Cos/J
View Strains carrying other alleles of Ret     (1 strain)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- 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).
Hirschsprung Disease, Susceptibility to, 1; HSCR1
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Central Hypoventilation Syndrome, Congenital; CCHS   (RET)
Multiple Endocrine Neoplasia, Type IIA; MEN2A   (RET)
Multiple Endocrine Neoplasia, Type IIB; MEN2B   (RET)
Pheochromocytoma Pheochromocytoma, Susceptibility to   (RET)
Rearranged During Transfection Protooncogene; RET   (RET)
Renal Hypodysplasia/Aplasia 1; RHDA1   (RET)
Thyroid Carcinoma, Familial Medullary; MTC   (RET)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

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

Rettm1Cos/Ret+

        involves: 129S/SvEv * C57BL/6
  • digestive/alimentary phenotype
  • intestinal hypoperistalsis
    • decrease in both longitudinal and circular muscle contraction of the intestine in response to electric field stimulation   (MGI Ref ID J:82456)
  • nervous system phenotype
  • abnormal enteric neuron morphology
    • colon submucosal neuron size is reduced by 16%, however cell size of small bowel submucosal neurons and myenteric and submucosal neuron numbers in the small bowel and colon are normal   (MGI Ref ID J:82456)
    • the myenteric plexus has a 35% reduction in cell size in the small bowel and 34% reduction in the colon   (MGI Ref ID J:82456)
    • myenteric neuron acetylcholinesterase-stained fiber counts are reduced by 11-13%   (MGI Ref ID J:82456)
  • abnormal neurotransmitter secretion
    • 70-95% reduction in substance P and VIP release   (MGI Ref ID J:82456)

Rettm1Cos/Ret+

        involves: 129S/SvEv * 129S1/Sv * 129X1/SvJ
  • renal/urinary system phenotype
  • decreased renal glomerulus number
    • at P15, heterozygotes show a reduced mean glomerular density relative to wild-type littermates (7.25 versus 8.95 glomeruli per unit area, respectively)   (MGI Ref ID J:117753)
  • single kidney
    • at P15, about 4% of heterozygotes exhibit unilateral renal agenesis   (MGI Ref ID J:117753)

Rettm1Cos/Rettm1Cos

        involves: 129S/SvEv * MF1
  • mortality/aging
  • complete neonatal lethality   (MGI Ref ID J:30389)
    • death occurred 16-24 hours after birth   (MGI Ref ID J:23852)
  • cardiovascular system phenotype
  • *normal* cardiovascular system phenotype
    • no gross abnormalities, the ventricles, atria, valves, aorta and pulmonary trunk showed no defects   (MGI Ref ID J:64539)
  • digestive/alimentary phenotype
  • intestinal hypoperistalsis   (MGI Ref ID J:30389)
    • failure of milk to progress from the stomach to the intestine   (MGI Ref ID J:23852)
  • endocrine/exocrine gland phenotype
  • *normal* endocrine/exocrine gland phenotype
    • adrenal chromaffin cells develop normally, despite high levels of Ret expression occuring in normal development of these cells   (MGI Ref ID J:82111)
  • renal/urinary system phenotype
  • abnormal branching involved in ureteric bud morphogenesis
    • of those buds that entered the mesenchyme, the growth and branching was abnormal, if occuring at all   (MGI Ref ID J:84282)
  • abnormal kidney morphology
    • remaining kidney rudiments are dysplastic with few nephric elements (proximal and distal tubules, glomeruli, and vessels) and no recognizable medulla, cortex, or nephrogenic zone   (MGI Ref ID J:23852)
    • dysplastic   (MGI Ref ID J:30389)
    • abnormal kidney collecting duct morphology
      • absence of mature collecting ducts   (MGI Ref ID J:23852)
    • abnormal kidney mesenchyme morphology
      • persistence of large regions of undifferentiated mesenchyme   (MGI Ref ID J:23852)
      • abnormal metanephric mesenchyme morphology
        • the metanephric mesenchyme did not condense by E11.5   (MGI Ref ID J:84282)
        • increased metanephric mesenchyme apoptosis
          • the metanephric mesenchyme underwent apoptosis at E12.5   (MGI Ref ID J:84282)
    • absent kidney
      • variable penetrance   (MGI Ref ID J:30389)
      • variable penetrance; kidneys are absent or rudimetary; both unilateral and bilateral effects were observed   (MGI Ref ID J:23852)
    • absent nephrogenic zone
      • no recognizable nephrogenic zone   (MGI Ref ID J:23852)
    • dilated renal glomerular capsule   (MGI Ref ID J:30389)
    • dilated renal tubules   (MGI Ref ID J:30389)
    • small kidney
      • rudimetary and are of similar size to the adrenal glands when present   (MGI Ref ID J:30389)
  • abnormal ureter morphology
    • sometimes absent or blind-ending   (MGI Ref ID J:30389)
    • variable severity; some animals exhibited an absent ureter and kidney, while others exhibited blind ureters with no renal tissue   (MGI Ref ID J:23852)
    • abnormal ureter development
      • reduced branching of the ureter   (MGI Ref ID J:23852)
    • absent ureter   (MGI Ref ID J:23852)
      • sometimes absent   (MGI Ref ID J:30389)
    • blind ureter   (MGI Ref ID J:23852)
      • sometimes blind-ending   (MGI Ref ID J:30389)
  • abnormal ureteric bud elongation
    • when the uteric bud was present, growth was retarded   (MGI Ref ID J:84282)
    • abnormal ureteric bud invasion
      • in approximately half of the mutant embryos, the uteric bud failed to evaginate although a mesenchymal blastema and a Wollfian duct were present in metanephroi   (MGI Ref ID J:84282)
      • when the uteric bud was present, growth was retarded and either failed to enter the mesenchyme or was delayed; at E11.0, 8% of the mutant buds had entered the mesenchyme   (MGI Ref ID J:84282)
  • respiratory system phenotype
  • abnormal lung development
    • underdeveloped or collapsed lungs; likely a secondary effect of deficient amniotic fluid production by the kidneys   (MGI Ref ID J:30389)
  • nervous system phenotype
  • abnormal cardiac ganglion morphology
    • cardiac ganglion volume was 56% smaller than controls, due to a reduction in neuronal cell number   (MGI Ref ID J:64539)
  • abnormal parasympathetic postganglionic fiber morphology
    • in two of six hearts, the AV node, the AV bundle and the proximal bundle branches were devoid of cholinergic fibers   (MGI Ref ID J:64539)
  • abnormal stellate ganglion morphology
    • occasionally larger than in controls   (MGI Ref ID J:30830)
  • absent enteric neurons   (MGI Ref ID J:30389)
    • no neurons in the small or large intestine, esophagus or stomach   (MGI Ref ID J:23852)
    • neurons and glia were absent from the distal stomach, duodenum, small and large intestine, but not the esophagus or the proximal stomach as determined by TH, NF or MASH-1 immunoreactivity   (MGI Ref ID J:30830)
  • absent superior cervical ganglion
    • absent as early as E12.5, while all other sympathetic ganglia were present   (MGI Ref ID J:30830)
  • embryogenesis phenotype
  • abnormal enteric neural crest cell migration
    • mutant enteric crest cells were detected in the esophagus and proximal stomach, but not the rest of the gastrointestinal tract   (MGI Ref ID J:30830)
  • abnormal mesonephros morphology
    • reduced numbers of mesonephric tubules were observed at E11.5   (MGI Ref ID J:84282)
  • cellular phenotype
  • abnormal enteric neural crest cell migration
    • mutant enteric crest cells were detected in the esophagus and proximal stomach, but not the rest of the gastrointestinal tract   (MGI Ref ID J:30830)
  • increased metanephric mesenchyme apoptosis
    • the metanephric mesenchyme underwent apoptosis at E12.5   (MGI Ref ID J:84282)
  • homeostasis/metabolism phenotype
  • oligohydramnios
    • deficient amniotic fluid production by the kidneys   (MGI Ref ID J:30389)

Rettm1Cos/Rettm1Cos

        involves: 129S/Sv * C57BL/6
  • nervous system phenotype
  • abnormal enteric nervous system morphology
    • absence of neurofilament labeling in latissimus dorsi muscle of P0 mice   (MGI Ref ID J:135153)
    • abnormal enteric ganglia morphology
      • display a nearly complete absence of the enteric ganglia throughout the entire gastrointestinal tract   (MGI Ref ID J:135153)
  • renal/urinary system phenotype
  • absent kidney   (MGI Ref ID J:135153)
View Research Applications

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

Cardiovascular Research
Heart Abnormalities

Cell Biology Research
Signal Transduction

Developmental Biology Research
Internal/Organ Defects
      heart
      kidney
      megacolon
      multiple
      urogenital
Mesodermal Defects
Neural Crest Defects
Neurodevelopmental Defects
Perinatal Lethality
      Homozygous

Internal/Organ Research
Gastrointestinal Defects
Heart Abnormalities
Kidney Defects

Neurobiology Research
Neural Tube Defects
Neurodevelopmental Defects

Research Tools
Developmental Biology Research

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Rettm1Cos
Allele Name targeted mutation 1, Frank Costantini
Allele Type Targeted (Null/Knockout)
Common Name(s) Ret-; c-ret-; ret-k-;
Mutation Made By Frank Costantini,   Columbia University Medical Center
Strain of Origin129S/SvEv-Gpi1
Gene Symbol and Name Ret, ret proto-oncogene
Chromosome 6
Gene Common Name(s) CDHF12; CDHR16; HSCR1; MEN2A; MEN2B; MTC1; PTC; RET-ELE1; RET51; RET9; c-Ret;
Molecular Note A neomycin resistance cassette replaced 0.8 kb of sequence, including the codon for an invariant lysine required for kinase activity. Northern blot analysis did not detect normal transcripts in brains of homozygous mice, but did detect several transcripts with sizes consistent with predicted products of the mutant allele. [MGI Ref ID J:23852]

Genotyping

Genotyping Information

Genotyping Protocols

Rettm1Cos, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Schuchardt A; D'Agati V; Larsson-Blomberg L; Costantini F; Pachnis V. 1994. Defects in the kidney and enteric nervous system of mice lacking the tyrosine kinase receptor Ret [see comments] Nature 367(6461):380-3. [PubMed: 8114940]  [MGI Ref ID J:23852]

Additional References

Rettm1Cos related

Aizenfisz S; Dauger S; Durand E; Vardon G; Levacher B; Simonneau M; Pachnis V; Gaultier C; Gallego J. 2002. Ventilatory responses to hypercapnia and hypoxia in heterozygous c-ret newborn mice. Respir Physiol Neurobiol 131(3):213-22. [PubMed: 12126922]  [MGI Ref ID J:102807]

Allmendinger A; Stoeckel E; Saarma M; Unsicker K; Huber K. 2003. Development of adrenal chromaffin cells is largely normal in mice lacking the receptor tyrosine kinase c-Ret. Mech Dev 120(3):299-304. [PubMed: 12591599]  [MGI Ref ID J:82111]

Almeida AR; Arroz-Madeira S; Fonseca-Pereira D; Ribeiro H; Lasrado R; Pachnis V; Veiga-Fernandes H. 2012. RET/GFRalpha signals are dispensable for thymic T cell development in vivo. PLoS One 7(12):e52949. [PubMed: 23300832]  [MGI Ref ID J:195828]

Ashrafi S; Lalancette-Hebert M; Friese A; Sigrist M; Arber S; Shneider NA; Kaltschmidt JA. 2012. Wnt7A Identifies Embryonic gamma-Motor Neurons and Reveals Early Postnatal Dependence of gamma-Motor Neurons on a Muscle Spindle-Derived Signal. J Neurosci 32(25):8725-8731. [PubMed: 22723712]  [MGI Ref ID J:185656]

Barlow A; de Graaff E; Pachnis V. 2003. Enteric nervous system progenitors are coordinately controlled by the G protein-coupled receptor EDNRB and the receptor tyrosine kinase RET. Neuron 40(5):905-16. [PubMed: 14659090]  [MGI Ref ID J:130623]

Batourina E; Choi C; Paragas N; Bello N; Hensle T; Costantini FD; Schuchardt A; Bacallao RL; Mendelsohn CL. 2002. Distal ureter morphogenesis depends on epithelial cell remodeling mediated by vitamin A and Ret. Nat Genet 32(1):109-15. [PubMed: 12195422]  [MGI Ref ID J:78712]

Bonanomi D; Chivatakarn O; Bai G; Abdesselem H; Lettieri K; Marquardt T; Pierchala BA; Pfaff SL. 2012. Ret Is a Multifunctional Coreceptor that Integrates Diffusible- and Contact-Axon Guidance Signals. Cell 148(3):568-82. [PubMed: 22304922]  [MGI Ref ID J:180801]

Brophy PD; Ostrom L; Lang KM; Dressler GR. 2001. Regulation of ureteric bud outgrowth by Pax2-dependent activation of the glial derived neurotrophic factor gene. Development 128(23):4747-56. [PubMed: 11731455]  [MGI Ref ID J:72723]

Burau K; Stenull I; Huber K; Misawa H; Berse B; Unsicker K; Ernsberger U. 2004. c-ret regulates cholinergic properties in mouse sympathetic neurons: evidence from mutant mice. Eur J Neurosci 20(2):353-62. [PubMed: 15233745]  [MGI Ref ID J:92351]

Carrasquillo MM; McCallion AS; Puffenberger EG; Kashuk CS; Nouri N; Chakravarti A. 2002. Genome-wide association study and mouse model identify interaction between RET and EDNRB pathways in Hirschsprung disease. Nat Genet 32(2):237-44. [PubMed: 12355085]  [MGI Ref ID J:112429]

Chi X; Michos O; Shakya R; Riccio P; Enomoto H; Licht JD; Asai N; Takahashi M; Ohgami N; Kato M; Mendelsohn C; Costantini F. 2009. Ret-dependent cell rearrangements in the Wolffian duct epithelium initiate ureteric bud morphogenesis. Dev Cell 17(2):199-209. [PubMed: 19686681]  [MGI Ref ID J:152967]

Chia I; Grote D; Marcotte M; Batourina E; Mendelsohn C; Bouchard M. 2011. Nephric duct insertion is a crucial step in urinary tract maturation that is regulated by a Gata3-Raldh2-Ret molecular network in mice. Development 138(10):2089-97. [PubMed: 21521737]  [MGI Ref ID J:171426]

Clarke JC; Patel SR; Raymond RM Jr; Andrew S; Robinson BG; Dressler GR; Brophy PD. 2006. Regulation of c-Ret in the developing kidney is responsive to Pax2 gene dosage. Hum Mol Genet 15(23):3420-8. [PubMed: 17047028]  [MGI Ref ID J:117753]

Durbec PL; Larsson-Blomberg LB; Schuchardt A; Costantini F; Pachnis V. 1996. Common origin and developmental dependence on c-ret of subsets of enteric and sympathetic neuroblasts. Development 122(1):349-58. [PubMed: 8565847]  [MGI Ref ID J:30830]

Enomoto H; Heuckeroth RO; Golden JP; Johnson EM; Milbrandt J. 2000. Development of cranial parasympathetic ganglia requires sequential actions of GDNF and neurturin. Development 127(22):4877-89. [PubMed: 11044402]  [MGI Ref ID J:114185]

Euteneuer S; Yang KH; Chavez E; Leichtle A; Loers G; Olshansky A; Pak K; Schachner M; Ryan AF. 2013. Glial cell line-derived neurotrophic factor (GDNF) induces neuritogenesis in the cochlear spiral ganglion via neural cell adhesion molecule (NCAM). Mol Cell Neurosci 54:30-43. [PubMed: 23262364]  [MGI Ref ID J:203649]

Gianino S; Grider JR; Cresswell J; Enomoto H; Heuckeroth RO. 2003. GDNF availability determines enteric neuron number by controlling precursor proliferation. Development 130(10):2187-98. [PubMed: 12668632]  [MGI Ref ID J:82456]

Grote D; Boualia SK; Souabni A; Merkel C; Chi X; Costantini F; Carroll T; Bouchard M. 2008. Gata3 acts downstream of beta-catenin signaling to prevent ectopic metanephric kidney induction. PLoS Genet 4(12):e1000316. [PubMed: 19112489]  [MGI Ref ID J:142876]

Hiltunen JO; Laurikainen A; Airaksinen MS; Saarma M. 2000. GDNF family receptors in the embryonic and postnatal rat heart and reduced cholinergic innervation in mice hearts lacking ret or GFRalpha2. Dev Dyn 219(1):28-39. [PubMed: 10974669]  [MGI Ref ID J:64539]

Huang T; Hu J; Wang B; Nie Y; Geng J; Cheng L. 2013. Tlx3 controls cholinergic transmitter and Peptide phenotypes in a subset of prenatal sympathetic neurons. J Neurosci 33(26):10667-75. [PubMed: 23804090]  [MGI Ref ID J:199638]

Kitagaki J; Ueda Y; Chi X; Sharma N; Elder CM; Truffer E; Costantini F; Lewandoski M; Perantoni AO. 2011. FGF8 is essential for formation of the ductal system in the male reproductive tract. Development 138(24):5369-78. [PubMed: 22110055]  [MGI Ref ID J:178935]

Kuure S; Cebrian C; Machingo Q; Lu BC; Chi X; Hyink D; D'Agati V; Gurniak C; Witke W; Costantini F. 2010. Actin depolymerizing factors cofilin1 and destrin are required for ureteric bud branching morphogenesis. PLoS Genet 6(10):e1001176. [PubMed: 21060807]  [MGI Ref ID J:167529]

Ledda F; Paratcha G; Sandoval-Guzman T; Ibanez CF. 2007. GDNF and GFRalpha1 promote formation of neuronal synapses by ligand-induced cell adhesion. Nat Neurosci 10(3):293-300. [PubMed: 17310246]  [MGI Ref ID J:120732]

Majumdar A; Vainio S; Kispert A; McMahon J; McMahon AP. 2003. Wnt11 and Ret/Gdnf pathways cooperate in regulating ureteric branching during metanephric kidney development. Development 130(14):3175-85. [PubMed: 12783789]  [MGI Ref ID J:83430]

Michos O; Cebrian C; Hyink D; Grieshammer U; Williams L; D'Agati V; Licht JD; Martin GR; Costantini F. 2010. Kidney development in the absence of Gdnf and Spry1 requires Fgf10. PLoS Genet 6(1):e1000809. [PubMed: 20084103]  [MGI Ref ID J:156865]

Ngan ES; Shum CK; Poon HC; Sham MH; Garcia-Barcelo MM; Lui VC; Tam PK. 2008. Prokineticin-1 (Prok-1) works coordinately with glial cell line-derived neurotrophic factor (GDNF) to mediate proliferation and differentiation of enteric neural crest cells. Biochim Biophys Acta 1783(3):467-78. [PubMed: 18006159]  [MGI Ref ID J:133292]

Ola R; Jakobson M; Kvist J; Perala N; Kuure S; Braunewell KH; Bridgewater D; Rosenblum ND; Chilov D; Immonen T; Sainio K; Sariola H. 2011. The GDNF target Vsnl1 marks the ureteric tip. J Am Soc Nephrol 22(2):274-84. [PubMed: 21289216]  [MGI Ref ID J:191040]

Pozas E; Ibanez CF. 2005. GDNF and GFRalpha1 promote differentiation and tangential migration of cortical GABAergic neurons. Neuron 45(5):701-13. [PubMed: 15748846]  [MGI Ref ID J:99763]

Rossi J; Tomac A; Saarma M; Airaksinen MS. 2000. Distinct roles for GFRalpha1 and GFRalpha2 signalling in different cranial parasympathetic ganglia in vivo. Eur J Neurosci 12(11):3944-52. [PubMed: 11069590]  [MGI Ref ID J:89887]

Rothman TP; Chen J; Howard MJ; Costantini F; Schuchardt A; Pachnis V; Gershon MD. 1996. Increased expression of laminin-1 and collagen (IV) subunits in the aganglionic bowel of ls/ls, but not c-ret -/- mice. Dev Biol 178(2):498-513. [PubMed: 8812145]  [MGI Ref ID J:35512]

Schuchardt A; D'Agati V; Larsson-Blomberg L; Costantini F; Pachnis V. 1995. RET-deficient mice: an animal model for Hirschsprung's disease and renal agenesis. J Intern Med 238(4):327-32. [PubMed: 7595168]  [MGI Ref ID J:30389]

Schuchardt A; D'Agati V; Pachnis V; Costantini F. 1996. Renal agenesis and hypodysplasia in ret-k- mutant mice result from defects in ureteric bud development. Development 122(6):1919-29. [PubMed: 8674430]  [MGI Ref ID J:84282]

Shakya R; Watanabe T; Costantini F. 2005. The role of GDNF/Ret signaling in ureteric bud cell fate and branching morphogenesis. Dev Cell 8(1):65-74. [PubMed: 15621530]  [MGI Ref ID J:95805]

Song MR; Shirasaki R; Cai CL; Ruiz EC; Evans SM; Lee SK; Pfaff SL. 2006. T-Box transcription factor Tbx20 regulates a genetic program for cranial motor neuron cell body migration. Development 133(24):4945-55. [PubMed: 17119020]  [MGI Ref ID J:119655]

Srinivas S; Wu Z; Chen CM; D'Agati V; Costantini F. 1999. Dominant effects of RET receptor misexpression and ligand-independent RET signaling on ureteric bud development. Development 126(7):1375-86. [PubMed: 10068631]  [MGI Ref ID J:52988]

Taraviras S; Marcos-Gutierrez CV; Durbec P; Jani H; Grigoriou M ; Sukumaran M ; Wang LC ; Hynes M ; Raisman G ; Pachnis V. 1999. Signalling by the RET receptor tyrosine kinase and its role in the development of the mammalian enteric nervous system. Development 126(12):2785-97. [PubMed: 10331988]  [MGI Ref ID J:54981]

Uesaka T; Nagashimada M; Yonemura S; Enomoto H. 2008. Diminished Ret expression compromises neuronal survival in the colon and causes intestinal aganglionosis in mice. J Clin Invest 118(5):1890-8. [PubMed: 18414682]  [MGI Ref ID J:135153]

Veiga-Fernandes H; Coles MC; Foster KE; Patel A; Williams A; Natarajan D; Barlow A; Pachnis V; Kioussis D. 2007. Tyrosine kinase receptor RET is a key regulator of Peyer's patch organogenesis. Nature 446(7135):547-51. [PubMed: 17322904]  [MGI Ref ID J:120816]

Viemari JC; Maussion G; Bevengut M; Burnet H; Pequignot JM; Nepote V; Pachnis V; Simonneau M; Hilaire G. 2005. Ret deficiency in mice impairs the development of A5 and A6 neurons and the functional maturation of the respiratory rhythm. Eur J Neurosci 22(10):2403-12. [PubMed: 16307583]  [MGI Ref ID J:103324]

de Graaff E; Srinivas S; Kilkenny C; D'Agati V; Mankoo BS; Costantini F; Pachnis V. 2001. Differential activities of the RET tyrosine kinase receptor isoforms during mammalian embryogenesis. Genes Dev 15(18):2433-44. [PubMed: 11562352]  [MGI Ref ID J:71588]

Health & husbandry

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.

Health & Colony Maintenance Information

Animal Health Reports

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

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, heterozygous mice may be bred together, to wildtype siblings or to 129S1/SvImJ inbred mice (Stock No. 002448). Homozygous mice die around one day after birth.

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* $3300.00
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 willfulfill 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 10 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* $4290.00
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 willfulfill 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 10 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.

Control Information

  Control
   Wild-type from the colony
   002448 129S1/SvImJ
 
  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.


See Terms of Use tab for General Terms and Conditions


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.
Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.

Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

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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