Strain Name:

B6;129S7-Wnt5atm1Amc/J

Stock Number:

004758

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Availability:

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Homozygous null mice have a perinatal lethal phenotype and do not survive long after birth due to respiratory failure. Homozygous 17.5 to 18.5 embryonic day old embryos exhibit severe shortening in all outgrowing axes of the body and limbs with loss of distal structures (absence of tail, limb digits and genital tubercle), and truncated facial features. This mutant mouse strain may be useful in studies of distal outgrowth of internal organs and organization of morphogenesis in development.

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 Andrew P McMahon,   University of Southern California

Description
Homozygous null mice have a perinatal lethal phenotype and do not survive long after birth due to respiratory failure. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by immunohistochemical analysis in homozygotes. Homozygous 17.5 to 18.5 embryonic day old embryos exhibit severe shortening in all outgrowing axes of the body and limbs with loss of distal structures (absence of tail, limb digits and genital tubercle), and truncated facial features. Newborn homozygous mice succumb to asphyxia due to abnormal lung development and display shortened trachea, overexpansion of the distal airways and impaired capillary/alveolar coupling. This mutant mouse strain may be useful in studies of distal outgrowth of internal organs and organization of morphogenesis in development.

Development
A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt exon 2 at codon 31. The construct was electroporated into 129S7/SvEvBrd-derived AB1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts.

Control Information

  Control
   Wild-type from the colony
 
  Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Wnt5a
022938   FVB/N-Tg(tetO-Wnt5a)17Rva/J
View Strains carrying other alleles of Wnt5a     (1 strain)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.
Anorectal Anomalies
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Robinow Syndrome, Autosomal Dominant; DRS   (WNT5A)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Wnt5atm1Amc/Wnt5atm1Amc

        involves: 129S7/SvEvBrd * C57BL/6
  • mortality/aging
  • complete neonatal lethality   (MGI Ref ID J:78384)
    • live at birth but dead shortly thereafter   (MGI Ref ID J:52600)
  • craniofacial phenotype
  • decreased tongue size
    • tongue truncated   (MGI Ref ID J:52600)
  • short mandible   (MGI Ref ID J:52600)
  • short snout   (MGI Ref ID J:52600)
  • small ears
    • reduced outgrowth of external ears   (MGI Ref ID J:52600)
  • embryogenesis phenotype
  • abnormal embryonic tissue morphology
    • embryos examined at E17.5 to E18.5 showed gross morphological defects of outgrowing tissues   (MGI Ref ID J:52600)
    • abnormal presomitic mesoderm morphology
      • reduction in presomitic mesoderm, evident at E9.5   (MGI Ref ID J:52600)
    • decreased somite size
      • at E9.5, evident that caudal somites were smaller than controls   (MGI Ref ID J:52600)
      • same number of somites existed, however   (MGI Ref ID J:52600)
  • abnormal primitive streak formation
    • shortened, evident at E8.5   (MGI Ref ID J:52600)
  • growth/size/body phenotype
  • decreased body length
    • embryos examined at E17.5 to E18.5 were truncated caudally   (MGI Ref ID J:52600)
    • significant shortening of embryonic anterior-posterior axis   (MGI Ref ID J:52600)
  • hearing/vestibular/ear phenotype
  • small ears
    • reduced outgrowth of external ears   (MGI Ref ID J:52600)
  • limbs/digits/tail phenotype
  • absent caudal vertebrae   (MGI Ref ID J:52600)
  • adactyly
    • of both fore- and hindlimbs   (MGI Ref ID J:52600)
  • short humerus
    • 59% the length of littermate controls   (MGI Ref ID J:52600)
  • short limbs   (MGI Ref ID J:52600)
  • short radius
    • 30 to 40% the length of littermate controls   (MGI Ref ID J:52600)
  • short ulna
    • 30 to 40% the length of littermate controls   (MGI Ref ID J:52600)
  • vestigial tail   (MGI Ref ID J:52600)
  • reproductive system phenotype
  • abnormal reproductive system morphology   (MGI Ref ID J:52600)
    • absent external female genitalia   (MGI Ref ID J:52600)
    • absent external male genitalia   (MGI Ref ID J:52600)
  • respiratory system phenotype
  • abnormal lung development
    • hypercellular with thickened interstitium, evident at E18   (MGI Ref ID J:78384)
    • increased numbers of terminal airways, evident at E16   (MGI Ref ID J:78384)
    • overexpanded distal airways   (MGI Ref ID J:78384)
    • failed coupling of airways to lung capillaries   (MGI Ref ID J:78384)
    • differentiation of specialized lung epithelial cells was normal, however   (MGI Ref ID J:78384)
  • abnormal lung interstitium morphology
    • thickened, evident at E18   (MGI Ref ID J:78384)
  • decreased tracheal cartilage ring number
    • fewer cartilage rings than in littermate controls   (MGI Ref ID J:78384)
  • respiratory failure
    • neonatal death apparently due to respiratory failure   (MGI Ref ID J:78384)
  • short trachea
    • short, with fewer cartilage rings than littermate controls   (MGI Ref ID J:78384)
    • no evidence of tracheoesophogeal fusion or of abnormal cellular differentation   (MGI Ref ID J:78384)
  • skeleton phenotype
  • abnormal vertebrae morphology
    • abnormalities increased in severity caudally   (MGI Ref ID J:52600)
    • absent caudal vertebrae   (MGI Ref ID J:52600)
    • small vertebrae   (MGI Ref ID J:52600)
    • vertebral fusion   (MGI Ref ID J:52600)
  • decreased tracheal cartilage ring number
    • fewer cartilage rings than in littermate controls   (MGI Ref ID J:78384)
  • delayed bone ossification
    • in proximal limb elements   (MGI Ref ID J:52600)
    • absent in radius and metacarpals   (MGI Ref ID J:52600)
  • rib fusion   (MGI Ref ID J:52600)
  • short humerus
    • 59% the length of littermate controls   (MGI Ref ID J:52600)
  • short mandible   (MGI Ref ID J:52600)
  • short radius
    • 30 to 40% the length of littermate controls   (MGI Ref ID J:52600)
  • short ulna
    • 30 to 40% the length of littermate controls   (MGI Ref ID J:52600)
  • short vertebral column
    • length of vertebral column was 1/2 that of littermate controls   (MGI Ref ID J:78384)
  • digestive/alimentary phenotype
  • decreased tongue size
    • tongue truncated   (MGI Ref ID J:52600)

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

Wnt5atm1Amc/Wnt5atm1Amc

        involves: 129S7/SvEvBrd
  • digestive/alimentary phenotype
  • abnormal anus morphology
    • at E18.5, all mice exhibit anorectal malformations and fail to show continuity of the rectum and anal epithelium unlike in wild-type mice   (MGI Ref ID J:153152)
    • absent anus   (MGI Ref ID J:153152)
    • anal atresia
  • abnormal colon morphology
    • at E15.5, mice exhibit a fistula between the bladder and the colon unlike wild-type mice   (MGI Ref ID J:153152)
    • at E18.5, only 25% of mice display a fistula between the bladder and colon unlike in wild-type mice   (MGI Ref ID J:153152)
    • most mice exhibit a blind-ending pouch without a fistula unlike in wild-type mice   (MGI Ref ID J:153152)
    • mice exhibit a shortening of the colon   (MGI Ref ID J:153152)
  • abnormal rectum morphology
    • at E18.5, all mice exhibit anorectal malformations and fail to show continuity of the rectum and anal epithelium unlike in wild-type mice   (MGI Ref ID J:153152)
    • absent rectum
      • mice lack rectal tissues   (MGI Ref ID J:153152)
  • renal/urinary system phenotype
  • abnormal urinary bladder morphology
    • at E15.5, mice exhibit a fistula between the bladder and the colon unlike wild-type mice   (MGI Ref ID J:153152)
    • at E18.5, only 25% of mice display a fistula between the bladder and colon unlike in wild-type mice   (MGI Ref ID J:153152)
    • most mice exhibit a blind-ending pouch without a fistula unlike in wild-type mice   (MGI Ref ID J:153152)
  • liver/biliary system phenotype
  • abnormal liver morphology
    • the liver is displaced caudally   (MGI Ref ID J:153152)
    • enlarged liver   (MGI Ref ID J:153152)
  • limbs/digits/tail phenotype
  • abnormal autopod morphology
  • short limbs   (MGI Ref ID J:153152)
  • short tail   (MGI Ref ID J:153152)
  • reproductive system phenotype
  • abnormal primordial germ cell apoptosis
    • increase in apoptosis of extragonadal primordial germ cells at E10.5 and E11.5   (MGI Ref ID J:179805)
  • abnormal primordial germ cell migration
    • fail to migrate rostrally at E10.5, remaining caudally distributed   (MGI Ref ID J:179805)
    • ectopic PGCs make up over 70% of the total PGCs at E11.5 compared to less than 5% in wild-type controls   (MGI Ref ID J:179805)
  • decreased primordial germ cell number
    • at E10.5, E11.5 and E12.5   (MGI Ref ID J:179805)
  • genital tubercle hypoplasia
    • at E18.5, the genital tubercle is hypoplastic compared to in wild-type mice   (MGI Ref ID J:153152)
  • growth/size/body phenotype
  • decreased body size   (MGI Ref ID J:153152)
  • nervous system phenotype
  • *normal* nervous system phenotype
    • mice exhibit normal numbers of thoracic motor neurons and proportions of motor columnar subtypes   (MGI Ref ID J:155074)
  • cellular phenotype
  • abnormal primordial germ cell apoptosis
    • increase in apoptosis of extragonadal primordial germ cells at E10.5 and E11.5   (MGI Ref ID J:179805)
  • abnormal primordial germ cell migration
    • fail to migrate rostrally at E10.5, remaining caudally distributed   (MGI Ref ID J:179805)
    • ectopic PGCs make up over 70% of the total PGCs at E11.5 compared to less than 5% in wild-type controls   (MGI Ref ID J:179805)
View Research Applications

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

Wnt5atm1Amc related

Developmental Biology Research
Craniofacial and Palate Defects
Internal/Organ Defects
      lung
Perinatal Lethality
      Homozygous
Skeletal Defects
      truncated forelimbs, no hind limbs

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Wnt5atm1Amc
Allele Name targeted mutation 1, Andrew P McMahon
Allele Type Targeted (knock-out)
Common Name(s) Wnt5a-;
Mutation Made By Andrew McMahon,   University of Southern California
Strain of Origin129S7/SvEvBrd-Hprt<+>
ES Cell Line NameAB1
ES Cell Line Strain129S7/SvEvBrd-Hprt<+>
Gene Symbol and Name Wnt5a, wingless-related MMTV integration site 5A
Chromosome 14
Gene Common Name(s) 8030457G12Rik; RIKEN cDNA 8030457G12 gene; Wnt-5a; hWNT5A;
Molecular Note Exon 2 was disrupted at codon 31 by the insertion of a neomycin selection cassette. [MGI Ref ID J:52600]

Genotyping

Genotyping Information

Genotyping Protocols

Wnt5atm1Amc, Melt Curve Analysis
Wnt5atm1Amc, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Yamaguchi TP; Bradley A; McMahon AP; Jones S. 1999. A Wnt5a pathway underlies outgrowth of multiple structures in the vertebrate embryo. Development 126(6):1211-23. [PubMed: 10021340]  [MGI Ref ID J:52600]

Additional References

Li C; Xiao J; Hormi K; Borok Z; Minoo P. 2002. Wnt5a participates in distal lung morphogenesis. Dev Biol 248(1):68-81. [PubMed: 12142021]  [MGI Ref ID J:78384]

Wnt5atm1Amc related

Adameyko I; Lallemend F; Furlan A; Zinin N; Aranda S; Kitambi SS; Blanchart A; Favaro R; Nicolis S; Lubke M; Muller T; Birchmeier C; Suter U; Zaitoun I; Takahashi Y; Ernfors P. 2012. Sox2 and Mitf cross-regulatory interactions consolidate progenitor and melanocyte lineages in the cranial neural crest. Development 139(2):397-410. [PubMed: 22186729]  [MGI Ref ID J:178973]

Agalliu D; Takada S; Agalliu I; McMahon AP; Jessell TM. 2009. Motor neurons with axial muscle projections specified by Wnt4/5 signaling. Neuron 61(5):708-20. [PubMed: 19285468]  [MGI Ref ID J:155074]

Allgeier SH; Lin TM; Vezina CM; Moore RW; Fritz WA; Chiu SY; Zhang C; Peterson RE. 2008. WNT5A selectively inhibits mouse ventral prostate development. Dev Biol 324(1):10-7. [PubMed: 18804104]  [MGI Ref ID J:142714]

Andersson ER; Bryjova L; Biris K; Yamaguchi TP; Arenas E; Bryja V. 2009. Genetic interaction between Lrp6 and Wnt5a during mouse development. Dev Dyn 239(1):237-245. [PubMed: 19795512]  [MGI Ref ID J:155226]

Andersson ER; Prakash N; Cajanek L; Minina E; Bryja V; Bryjova L; Yamaguchi TP; Hall AC; Wurst W; Arenas E. 2008. Wnt5a regulates ventral midbrain morphogenesis and the development of A9-A10 dopaminergic cells in vivo. PLoS ONE 3(10):e3517. [PubMed: 18953410]  [MGI Ref ID J:144081]

Andersson ER; Salto C; Villaescusa JC; Cajanek L; Yang S; Bryjova L; Nagy II; Vainio SJ; Ramirez C; Bryja V; Arenas E. 2013. Wnt5a cooperates with canonical Wnts to generate midbrain dopaminergic neurons in vivo and in stem cells. Proc Natl Acad Sci U S A 110(7):E602-10. [PubMed: 23324743]  [MGI Ref ID J:193686]

Blakely BD; Bye CR; Fernando CV; Horne MK; Macheda ML; Stacker SA; Arenas E; Parish CL. 2011. Wnt5a regulates midbrain dopaminergic axon growth and guidance. PLoS One 6(3):e18373. [PubMed: 21483795]  [MGI Ref ID J:171436]

Bodmer D; Levine-Wilkinson S; Richmond A; Hirsh S; Kuruvilla R. 2009. Wnt5a mediates nerve growth factor-dependent axonal branching and growth in developing sympathetic neurons. J Neurosci 29(23):7569-81. [PubMed: 19515925]  [MGI Ref ID J:149814]

Bryja V; Andersson ER; Schambony A; Esner M; Bryjova L; Biris KK; Hall AC; Kraft B; Cajanek L; Yamaguchi TP; Buckingham M; Arenas E. 2009. The extracellular domain of Lrp5/6 inhibits noncanonical Wnt signaling in vivo. Mol Biol Cell 20(3):924-36. [PubMed: 19056682]  [MGI Ref ID J:163977]

Buttler K; Becker J; Pukrop T; Wilting J. 2013. Maldevelopment of dermal lymphatics in Wnt5a-knockout-mice. Dev Biol 381(2):365-76. [PubMed: 23850867]  [MGI Ref ID J:200762]

Cervantes S; Yamaguchi TP; Hebrok M. 2009. Wnt5a is essential for intestinal elongation in mice. Dev Biol 326(2):285-94. [PubMed: 19100728]  [MGI Ref ID J:145166]

Cha KB; Douglas KR; Potok MA; Liang H; Jones SN; Camper SA. 2004. WNT5A signaling affects pituitary gland shape. Mech Dev 121(2):183-94. [PubMed: 15037319]  [MGI Ref ID J:90448]

Chawengsaksophak K; Svingen T; Ng ET; Epp T; Spiller CM; Clark C; Cooper H; Koopman P. 2012. Loss of Wnt5a disrupts primordial germ cell migration and male sexual development in mice. Biol Reprod 86(1):1-12. [PubMed: 21900680]  [MGI Ref ID J:185786]

Chen L; Fulcoli FG; Ferrentino R; Martucciello S; Illingworth EA; Baldini A. 2012. Transcriptional control in cardiac progenitors: Tbx1 interacts with the BAF chromatin remodeling complex and regulates Wnt5a. PLoS Genet 8(3):e1002571. [PubMed: 22438823]  [MGI Ref ID J:183479]

Cohen ED; Miller MF; Wang Z; Moon RT; Morrisey EE. 2012. Wnt5a and Wnt11 are essential for second heart field progenitor development. Development 139(11):1931-40. [PubMed: 22569553]  [MGI Ref ID J:184511]

Dale JK; Malapert P; Chal J; Vilhais-Neto G; Maroto M; Johnson T; Jayasinghe S; Trainor P; Herrmann B; Pourquie O. 2006. Oscillations of the snail genes in the presomitic mesoderm coordinate segmental patterning and morphogenesis in vertebrate somitogenesis. Dev Cell 10(3):355-66. [PubMed: 16516838]  [MGI Ref ID J:106622]

Fenstermaker AG; Prasad AA; Bechara A; Adolfs Y; Tissir F; Goffinet A; Zou Y; Pasterkamp RJ. 2010. Wnt/planar cell polarity signaling controls the anterior-posterior organization of monoaminergic axons in the brainstem. J Neurosci 30(47):16053-64. [PubMed: 21106844]  [MGI Ref ID J:166974]

Florian MC; Nattamai KJ; Dorr K; Marka G; Uberle B; Vas V; Eckl C; Andra I; Schiemann M; Oostendorp RA; Scharffetter-Kochanek K; Kestler HA; Zheng Y; Geiger H. 2013. A canonical to non-canonical Wnt signalling switch in haematopoietic stem-cell ageing. Nature 503(7476):392-6. [PubMed: 24141946]  [MGI Ref ID J:206757]

Gao B; Song H; Bishop K; Elliot G; Garrett L; English MA; Andre P; Robinson J; Sood R; Minami Y; Economides AN; Yang Y. 2011. Wnt signaling gradients establish planar cell polarity by inducing Vangl2 phosphorylation through Ror2. Dev Cell 20(2):163-76. [PubMed: 21316585]  [MGI Ref ID J:169766]

Gros J; Hu JK; Vinegoni C; Feruglio PF; Weissleder R; Tabin CJ. 2010. WNT5A/JNK and FGF/MAPK pathways regulate the cellular events shaping the vertebrate limb bud. Curr Biol 20(22):1993-2002. [PubMed: 21055947]  [MGI Ref ID J:166897]

He F; Xiong W; Yu X; Espinoza-Lewis R; Liu C; Gu S; Nishita M; Suzuki K; Yamada G; Minami Y; Chen Y. 2008. Wnt5a regulates directional cell migration and cell proliferation via Ror2-mediated noncanonical pathway in mammalian palate development. Development 135(23):3871-9. [PubMed: 18948417]  [MGI Ref ID J:144627]

Ho HY; Susman MW; Bikoff JB; Ryu YK; Jonas AM; Hu L; Kuruvilla R; Greenberg ME. 2012. Wnt5a-Ror-Dishevelled signaling constitutes a core developmental pathway that controls tissue morphogenesis. Proc Natl Acad Sci U S A 109(11):4044-51. [PubMed: 22343533]  [MGI Ref ID J:182150]

Hu B; Lefort K; Qiu W; Nguyen BC; Rajaram RD; Castillo E; He F; Chen Y; Angel P; Brisken C; Dotto GP. 2010. Control of hair follicle cell fate by underlying mesenchyme through a CSL-Wnt5a-FoxN1 regulatory axis. Genes Dev 24(14):1519-32. [PubMed: 20634318]  [MGI Ref ID J:161768]

Huang S; Zhu X; Liu Y; Tao Y; Feng G; He L; Guo X; Ma G. 2012. Wls is expressed in the epidermis and regulates embryonic hair follicle induction in mice. PLoS One 7(9):e45904. [PubMed: 23029304]  [MGI Ref ID J:191972]

Kim HJ; Schleiffarth JR; Jessurun J; Sumanas S; Petryk A; Lin S; Ekker SC. 2005. Wnt5 signaling in vertebrate pancreas development. BMC Biol 3:23. [PubMed: 16246260]  [MGI Ref ID J:112755]

Kiyohashi K; Kakinuma S; Kamiya A; Sakamoto N; Nitta S; Yamanaka H; Yoshino K; Fujiki J; Murakawa M; Kusano-Kitazume A; Shimizu H; Okamoto R; Azuma S; Nakagawa M; Asahina Y; Tanimizu N; Kikuchi A; Nakauchi H; Watanabe M. 2013. Wnt5a signaling mediates biliary differentiation of fetal hepatic stem/progenitor cells in mice. Hepatology 57(6):2502-13. [PubMed: 23386589]  [MGI Ref ID J:199204]

Kuss P; Kraft K; Stumm J; Ibrahim D; Vallecillo-Garcia P; Mundlos S; Stricker S. 2014. Regulation of cell polarity in the cartilage growth plate and perichondrium of metacarpal elements by HOXD13 and WNT5A. Dev Biol 385(1):83-93. [PubMed: 24161848]  [MGI Ref ID J:205338]

Laird DJ; Altshuler-Keylin S; Kissner MD; Zhou X; Anderson KV. 2011. Ror2 enhances polarity and directional migration of primordial germ cells. PLoS Genet 7(12):e1002428. [PubMed: 22216013]  [MGI Ref ID J:179805]

Li C; Xiao J; Hormi K; Borok Z; Minoo P. 2002. Wnt5a participates in distal lung morphogenesis. Dev Biol 248(1):68-81. [PubMed: 12142021]  [MGI Ref ID J:78384]

Liang H; Chen Q; Coles AH; Anderson SJ; Pihan G; Bradley A; Gerstein R; Jurecic R; Jones SN. 2003. Wnt5a inhibits B cell proliferation and functions as a tumor suppressor in hematopoietic tissue. Cancer Cell 4(5):349-60. [PubMed: 14667502]  [MGI Ref ID J:87524]

Lin M; Li L; Liu C; Liu H; He F; Yan F; Zhang Y; Chen Y. 2011. Wnt5a regulates growth, patterning, and odontoblast differentiation of developing mouse tooth. Dev Dyn 240(2):432-40. [PubMed: 21246660]  [MGI Ref ID J:167829]

Liu HX; Grosse AS; Iwatsuki K; Mishina Y; Gumucio DL; Mistretta CM. 2012. Separate and distinctive roles for Wnt5a in tongue, lingual tissue and taste papilla development. Dev Biol 361(1):39-56. [PubMed: 22024319]  [MGI Ref ID J:179217]

Liu W; Li L; Li G; Garritano F; Shanske A; Frenz DA. 2008. Coordinated molecular control of otic capsule differentiation: functional role of Wnt5a signaling and opposition by sfrp3 activity. Growth Factors 26(6):343-54. [PubMed: 18991062]  [MGI Ref ID J:143184]

Lu C; Wan Y; Cao J; Zhu X; Yu J; Zhou R; Yao Y; Zhang L; Zhao H; Li H; Zhao J; He L; Ma G; Yang X; Yao Z; Guo X. 2013. Wnt-mediated reciprocal regulation between cartilage and bone development during endochondral ossification. Bone 53(2):566-74. [PubMed: 23274346]  [MGI Ref ID J:193842]

Maeda K; Kobayashi Y; Udagawa N; Uehara S; Ishihara A; Mizoguchi T; Kikuchi Y; Takada I; Kato S; Kani S; Nishita M; Marumo K; Martin TJ; Minami Y; Takahashi N. 2012. Wnt5a-Ror2 signaling between osteoblast-lineage cells and osteoclast precursors enhances osteoclastogenesis. Nat Med 18(3):405-12. [PubMed: 22344299]  [MGI Ref ID J:181641]

Matsuyama M; Aizawa S; Shimono A. 2009. Sfrp controls apicobasal polarity and oriented cell division in developing gut epithelium. PLoS Genet 5(3):e1000427. [PubMed: 19300477]  [MGI Ref ID J:147041]

Mericskay M; Kitajewski J; Sassoon D. 2004. Wnt5a is required for proper epithelial-mesenchymal interactions in the uterus. Development 131(9):2061-72. [PubMed: 15073149]  [MGI Ref ID J:89366]

Naillat F; Prunskaite-Hyyrylainen R; Pietila I; Sormunen R; Jokela T; Shan J; Vainio SJ. 2010. Wnt4/5a signalling coordinates cell adhesion and entry into meiosis during presumptive ovarian follicle development. Hum Mol Genet 19(8):1539-50. [PubMed: 20106871]  [MGI Ref ID J:158526]

Oishi I; Suzuki H; Onishi N; Takada R; Kani S; Ohkawara B; Koshida I; Suzuki K; Yamada G; Schwabe GC; Mundlos S; Shibuya H; Takada S; Minami Y. 2003. The receptor tyrosine kinase Ror2 is involved in non-canonical Wnt5a/JNK signalling pathway. Genes Cells 8(7):645-54. [PubMed: 12839624]  [MGI Ref ID J:89972]

Potok MA; Cha KB; Hunt A; Brinkmeier ML; Leitges M; Kispert A; Camper SA. 2008. WNT signaling affects gene expression in the ventral diencephalon and pituitary gland growth. Dev Dyn 237(4):1006-20. [PubMed: 18351662]  [MGI Ref ID J:132979]

Qian D; Jones C; Rzadzinska A; Mark S; Zhang X; Steel KP; Dai X; Chen P. 2007. Wnt5a functions in planar cell polarity regulation in mice. Dev Biol 306(1):121-33. [PubMed: 17433286]  [MGI Ref ID J:122585]

Roarty K; Serra R. 2007. Wnt5a is required for proper mammary gland development and TGF-{beta}-mediated inhibition of ductal growth. Development 134(21):3929-39. [PubMed: 17898001]  [MGI Ref ID J:126343]

Ryu YK; Collins SE; Ho HY; Zhao H; Kuruvilla R. 2013. An autocrine Wnt5a-Ror signaling loop mediates sympathetic target innervation. Dev Biol 377(1):79-89. [PubMed: 23454479]  [MGI Ref ID J:196291]

Sato A; Yamamoto H; Sakane H; Koyama H; Kikuchi A. 2010. Wnt5a regulates distinct signalling pathways by binding to Frizzled2. EMBO J 29(1):41-54. [PubMed: 19910923]  [MGI Ref ID J:156508]

Schleiffarth JR; Person AD; Martinsen BJ; Sukovich DJ; Neumann A; Baker CV; Lohr JL; Cornfield DN; Ekker SC; Petryk A. 2007. Wnt5a is required for cardiac outflow tract septation in mice. Pediatr Res 61(4):386-91. [PubMed: 17515859]  [MGI Ref ID J:161587]

Seifert AW; Yamaguchi T; Cohn MJ. 2009. Functional and phylogenetic analysis shows that Fgf8 is a marker of genital induction in mammals but is not required for external genital development. Development 136(15):2643-51. [PubMed: 19592577]  [MGI Ref ID J:158139]

Sinha T; Wang B; Evans S; Wynshaw-Boris A; Wang J. 2012. Disheveled mediated planar cell polarity signaling is required in the second heart field lineage for outflow tract morphogenesis. Dev Biol 370(1):135-44. [PubMed: 22841628]  [MGI Ref ID J:188039]

Stefater JA 3rd; Lewkowich I; Rao S; Mariggi G; Carpenter AC; Burr AR; Fan J; Ajima R; Molkentin JD; Williams BO; Wills-Karp M; Pollard JW; Yamaguchi T; Ferrara N; Gerhardt H; Lang RA. 2011. Regulation of angiogenesis by a non-canonical Wnt-Flt1 pathway in myeloid cells. Nature 474(7352):511-5. [PubMed: 21623369]  [MGI Ref ID J:173385]

Stump RJ; Ang S; Chen Y; von Bahr T; Lovicu FJ; Pinson K; de Iongh RU; Yamaguchi TP; Sassoon DA; McAvoy JW. 2003. A role for Wnt/beta-catenin signaling in lens epithelial differentiation. Dev Biol 259(1):48-61. [PubMed: 12812787]  [MGI Ref ID J:84052]

Suzuki K; Bachiller D; Chen YP; Kamikawa M; Ogi H; Haraguchi R; Ogino Y; Minami Y; Mishina Y; Ahn K; Crenshaw EB 3rd; Yamada G. 2003. Regulation of outgrowth and apoptosis for the terminal appendage: external genitalia: development by concerted actions of BMP signaling. (Erratum) Development 130(25):6209-20. [PubMed: 14602679]  [MGI Ref ID J:87225]

Tai CC; Sala FG; Ford HR; Wang KS; Li C; Minoo P; Grikscheit TC; Bellusci S. 2009. Wnt5a knock-out mouse as a new model of anorectal malformation. J Surg Res 156(2):278-82. [PubMed: 19577771]  [MGI Ref ID J:153152]

Takahashi S; Watanabe T; Okada M; Inoue K; Ueda T; Takada I; Watabe T; Yamamoto Y; Fukuda T; Nakamura T; Akimoto C; Fujimura T; Hoshino M; Imai Y; Metzger D; Miyazono K; Minami Y; Chambon P; Kitamura T; Matsumoto T; Kato S. 2011. Noncanonical Wnt signaling mediates androgen-dependent tumor growth in a mouse model of prostate cancer. Proc Natl Acad Sci U S A 108(12):4938-43. [PubMed: 21383160]  [MGI Ref ID J:170092]

Vivancos V; Chen P; Spassky N; Qian D; Dabdoub A; Kelley M; Studer M; Guthrie S. 2009. Wnt activity guides facial branchiomotor neuron migration, and involves the PCP pathway and JNK and ROCK kinases. Neural Dev 4:7. [PubMed: 19210786]  [MGI Ref ID J:160731]

Wang B; Sinha T; Jiao K; Serra R; Wang J. 2011. Disruption of PCP signaling causes limb morphogenesis and skeletal defects and may underlie Robinow syndrome and brachydactyly type B. Hum Mol Genet 20(2):271-85. [PubMed: 20962035]  [MGI Ref ID J:166923]

Welsh IC; Thomsen M; Gludish DW; Alfonso-Parra C; Bai Y; Martin JF; Kurpios NA. 2013. Integration of left-right Pitx2 transcription and Wnt signaling drives asymmetric gut morphogenesis via Daam2. Dev Cell 26(6):629-44. [PubMed: 24091014]  [MGI Ref ID J:204986]

Wyngaarden LA; Vogeli KM; Ciruna BG; Wells M; Hadjantonakis AK; Hopyan S. 2010. Oriented cell motility and division underlie early limb bud morphogenesis. Development 137(15):2551-8. [PubMed: 20554720]  [MGI Ref ID J:168374]

Yang DH; Yoon JY; Lee SH; Bryja V; Andersson ER; Arenas E; Kwon YG; Choi KY. 2009. Wnt5a is required for endothelial differentiation of embryonic stem cells and vascularization via pathways involving both Wnt/beta-catenin and protein kinase Calpha. Circ Res 104(3):372-9. [PubMed: 19096028]  [MGI Ref ID J:163441]

Yang Y; Topol L; Lee H; Wu J. 2003. Wnt5a and Wnt5b exhibit distinct activities in coordinating chondrocyte proliferation and differentiation. Development 130(5):1003-15. [PubMed: 12538525]  [MGI Ref ID J:81355]

Yu H; Ye X; Guo N; Nathans J. 2012. Frizzled 2 and frizzled 7 function redundantly in convergent extension and closure of the ventricular septum and palate: evidence for a network of interacting genes. Development 139(23):4383-94. [PubMed: 23095888]  [MGI Ref ID J:189062]

Zhu X; Zhu H; Zhang L; Huang S; Cao J; Ma G; Feng G; He L; Yang Y; Guo X. 2012. Wls-mediated Wnts differentially regulate distal limb patterning and tissue morphogenesis. Dev Biol 365(2):328-38. [PubMed: 22377357]  [MGI Ref ID J:184918]

van Amerongen R; Fuerer C; Mizutani M; Nusse R. 2012. Wnt5a can both activate and repress Wnt/beta-catenin signaling during mouse embryonic development. Dev Biol 369(1):101-14. [PubMed: 22771246]  [MGI Ref ID J:187621]

von Gise A; Zhou B; Honor LB; Ma Q; Petryk A; Pu WT. 2011. WT1 regulates epicardial epithelial to mesenchymal transition through beta-catenin and retinoic acid signaling pathways. Dev Biol 356(2):421-31. [PubMed: 21663736]  [MGI Ref ID J:175466]

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 & HusbandryThe strain is maintained as a heterozygote. Homozygotes are not viable.

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* $2450.00
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* $3185.00
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.

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.


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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