JAX Mouse Strain Datasheet - 009085

129S/Sv-Ret^tm1Cos/J

Stock No:: 009085

Targeted Mutation

Cryo Recovery

Overview

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.

Donating Investigator

Frank Costantini, Columbia University Medical Center

Genetic overview

Genetic Background	Generation

Ret^tm1Cos

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Ret	ret proto-oncogene

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Research Applications

Cardiovascular Research
Cell Biology Research
Developmental Biology Research
Internal/Organ Research
Neurobiology Research
Research Tools

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Base Price

Starting at:

$2,595.00 Domestic price Cryo Recovery

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Details

Detailed 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-Gpi1^c 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 Suggestions

Wild-type from the colony
002448 129S1/SvImJ

Additional Information

Considerations for Choosing Controls

Selected References

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: J:23852

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Genetics

Ret^tm1Cos

Allele Symbol: Ret^tm1Cos

Allele Name	targeted mutation 1, Frank Costantini
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	Ret-; c-ret-; ret-k-
Gene Symbol and Name	Ret, ret proto-oncogene
Gene Synonym(s)	CDHF12; CDHR16; HSCR1; MEN2A; MEN2B; MTC1; PTC; RET-ELE1; RET51; RET9; c-Ret
Strain of Origin	129S/SvEv-Gpi1
Chromosome	6
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.
Mutations Made By	Frank Costantini, Columbia University Medical Center

Disease/Phenotype

Disease Terms

Research Areas By Genotype

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

Mammalian Phenotype Terms by Genotype

Genotype: Ret^tm1Cos/Ret^tm1Cos
involves: 129S/SvEv

endocrine/exocrine gland phenotype

endocrine/exocrine gland phenotype
- adrenal chromaffin cells develop normally, despite high levels of Ret expression occuring in normal development of these cells

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

Genotype: Ret^tm1Cos/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)

single kidney
- at P15, about 4% of heterozygotes exhibit unilateral renal agenesis

Genotype: Ret^tm1Cos/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

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
- myenteric neuron acetylcholinesterase-stained fiber counts are reduced by 11-13%
- the myenteric plexus has a 35% reduction in cell size in the small bowel and 34% reduction in the colon

abnormal neurotransmitter secretion
- 70-95% reduction in substance P and VIP release

Genotype: Ret^tm1Cos/Ret^tm1Cos
involves: 129S/Sv * C57BL/6

nervous system phenotype

abnormal enteric ganglia morphology
- display a nearly complete absence of the enteric ganglia throughout the entire gastrointestinal tract

abnormal enteric nervous system morphology
- absence of neurofilament labeling in latissimus dorsi muscle of P0 mice

renal/urinary system phenotype

absent kidney

Genotype: Ret^tm1Cos/Ret^tm1Cos
involves: 129S/SvEv * MF1

mortality/aging

neonatal lethality, complete penetrance
- death occurred 16-24 hours after birth

cardiovascular system phenotype

cardiovascular system phenotype
- no gross abnormalities, the ventricles, atria, valves, aorta and pulmonary trunk showed no defects

digestive/alimentary phenotype

intestinal hypoperistalsis
- failure of milk to progress from the stomach to the intestine

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

abnormal kidney collecting duct morphology
- absence of mature collecting ducts

abnormal kidney mesenchyme morphology
- persistence of large regions of undifferentiated mesenchyme

abnormal kidney morphology
- dysplastic
- remaining kidney rudiments are dysplastic with few nephric elements (proximal and distal tubules, glomeruli, and vessels) and no recognizable medulla, cortex, or nephrogenic zone

abnormal metanephric mesenchyme morphology
- the metanephric mesenchyme did not condense by E11.5

abnormal ureter development
- reduced branching of the ureter

abnormal ureter morphology
- sometimes absent or blind-ending
- variable severity; some animals exhibited an absent ureter and kidney, while others exhibited blind ureters with no renal tissue

abnormal ureteric bud elongation
- when the uteric bud was present, growth was retarded

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
- 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

absent kidney
- variable penetrance
- variable penetrance; kidneys are absent or rudimetary; both unilateral and bilateral effects were observed

absent nephrogenic zone
- no recognizable nephrogenic zone

absent ureter
- sometimes absent

blind ureter
- sometimes blind-ending

dilated renal glomerular capsule

dilated renal tubules

increased metanephric mesenchyme apoptosis
- the metanephric mesenchyme underwent apoptosis at E12.5

small kidney
- rudimetary and are of similar size to the adrenal glands when present

respiratory system phenotype

abnormal lung development
- underdeveloped or collapsed lungs; likely a secondary effect of deficient amniotic fluid production by the kidneys

nervous system phenotype

abnormal cardiac ganglion morphology
- cardiac ganglion volume was 56% smaller than controls, due to a reduction in neuronal cell number

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

abnormal stellate ganglion morphology
- occasionally larger than in controls

absent enteric neurons
- 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
- no neurons in the small or large intestine, esophagus or stomach

absent superior cervical ganglion
- absent as early as E12.5, while all other sympathetic ganglia were present

embryo 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

abnormal mesonephros morphology
- reduced numbers of mesonephric tubules were observed at E11.5

increased metanephric mesenchyme apoptosis
- the metanephric mesenchyme underwent apoptosis at E12.5

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

increased metanephric mesenchyme apoptosis
- the metanephric mesenchyme underwent apoptosis at E12.5

homeostasis/metabolism phenotype

oligohydramnios
- deficient amniotic fluid production by the kidneys

References

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: J:23852

Additional - Ret^tm1Cos 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: 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: 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: 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: 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: 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: 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: J:180801
Bondurand N; Southard-Smith EM. 2016. Mouse models of Hirschsprung disease and other developmental disorders of the enteric nervous system: Old and new players. Dev Biol 417(2):139-57. PubMed: 27370713 MGI: J:235629
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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: J:142876
Gt(ROSA)26SorWang L; Mongera A; Bonanomi D; Cyganek L; Pfaff SL; Nusslein-Volhard C; Marquardt T. 2014. A conserved axon type hierarchy governing peripheral nerve assembly. Development 141(9):1875-83. PubMed: 24700820 MGI: J:213337
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: 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: J:199638
Jiang Q; Arnold S; Heanue T; Kilambi KP; Doan B; Kapoor A; Ling AY; Sosa MX; Guy M; Jiang Q; Burzynski G; West K; Bessling S; Griseri P; Amiel J; Fernandez RM; Verheij JB; Hofstra RM; Borrego S; Lyonnet S; Ceccherini I; Gray JJ; Pachnis V; McCallion AS; Chakravarti A. 2015. Functional loss of semaphorin 3C and/or semaphorin 3D and their epistatic interaction with ret are critical to Hirschsprung disease liability. Am J Hum Genet 96(4):581-96. PubMed: 25839327 MGI: J:230339
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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: J:54981
Uesaka T; Nagashimada M; Enomoto H. 2015. Neuronal Differentiation in Schwann Cell Lineage Underlies Postnatal Neurogenesis in the Enteric Nervous System. J Neurosci 35(27):9879-88. PubMed: 26156989 MGI: J:224366
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: 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: 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: J:103324
Zhu S; Zhao C; Wu Y; Yang Q; Shao A; Wang T; Wu J; Yin Y; Li Y; Hou J; Zhang X; Zhou G; Gu X; Wang X; Bustelo XR; Zhou J. 2015. Identification of a Vav2-dependent mechanism for GDNF/Ret control of mesolimbic DAT trafficking. Nat Neurosci 18(8):1084-93. PubMed: 26147533 MGI: J:224528
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: J:71588

Service	Genotype	Price
	Heterozygous or wildtype for Ret<tm1Cos>

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Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Rettm1Cos

Allele Symbol: Rettm1Cos

Disease Terms

Research Areas By Genotype

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

Mammalian Phenotype Terms by Genotype

Genotype: Rettm1Cos/Rettm1Cosinvolves: 129S/SvEv

endocrine/exocrine gland phenotype

Genotype: Rettm1Cos/Ret+involves: 129S/SvEv * 129S1/Sv * 129X1/SvJ

renal/urinary system phenotype

Genotype: Rettm1Cos/Ret+involves: 129S/SvEv * C57BL/6

digestive/alimentary phenotype

nervous system phenotype

Genotype: Rettm1Cos/Rettm1Cosinvolves: 129S/Sv * C57BL/6

nervous system phenotype

renal/urinary system phenotype

Genotype: Rettm1Cos/Rettm1Cosinvolves: 129S/SvEv * MF1

mortality/aging

cardiovascular system phenotype

digestive/alimentary phenotype

renal/urinary system phenotype

respiratory system phenotype

nervous system phenotype

embryo phenotype

cellular phenotype

homeostasis/metabolism phenotype

References

Additional - Rettm1Cos related

Genotyping Protocols

Breeding Considerations

Citation

Animal Health Reports

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

Live Mouse

Cryorecovery - Pricing

Progeny testing is not required

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Licensing Information

JAX® Mice, Products & Services Conditions of Use

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Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Ret^tm1Cos

Allele Symbol: Ret^tm1Cos

Genotype: Ret^tm1Cos/Ret^tm1Cos
involves: 129S/SvEv

Genotype: Ret^tm1Cos/Ret⁺
involves: 129S/SvEv * 129S1/Sv * 129X1/SvJ

Genotype: Ret^tm1Cos/Ret⁺
involves: 129S/SvEv * C57BL/6

Genotype: Ret^tm1Cos/Ret^tm1Cos
involves: 129S/Sv * C57BL/6

Genotype: Ret^tm1Cos/Ret^tm1Cos
involves: 129S/SvEv * MF1

Additional - Ret^tm1Cos related