Strain Name:

129S-Ece1tm1Reh/J

Stock Number:

008864

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Homozygous Ece1 (endothelin converting enzyme 1) targeted mutant mice die before embryonic day 13.5 (E13.5) on a 129 genetic background. These mice closely resemble human DiGeorge syndrome patients who suffer multiple craniofacial and cardiovascular defects.

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 InvestigatorDr. Masashi Yanagisawa,   Southwestern Medical School

Description
Homozygous endothelin converting enzyme 1 targeted mutant mice die before embryonic day 13.5 (E13.5) on a 129 genetic background. Pre-morbid homozygous embryos exhibit peripheral vascular dilation and pericardial effusion, consistent with cardiac failure. There is marked congestion and dilation of the atria and peripheral vessles, as well as generalized edema. The embryos also exhibit severe craniofacial defects. Western blot and enzyme immunoassay confirm that expression of the gene is eliminated in homozygous embryos. These mice closely resemble human DiGeorge syndrome patients who suffer multiple craniofacial and cardiovascular defects.

Development
The exon immediately 5' to the one encoding the zinc-binding domain of the targeted gene was replaced with a neomycin resistance cassette driven by the RNA polymerase II promoter. SM1 129S6/SvEvTac-derived embryonic stem cells were used to create the mutation. Chimeric males were bred to 129S6/SvEvTac females and maintained on that background by the donating laboratory.

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).
Conotruncal Heart Malformations; CTHM
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Hirschsprung Disease, Cardiac Defects, and Autonomic Dysfunction   (ECE1)
Hypertension, Essential   (ECE1)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Ece1tm1Reh/Ece1tm1Reh

        involves: 129S6/SvEvTac
  • mortality/aging
  • partial embryonic lethality during organogenesis
    • most embryos die prior to E13.5   (MGI Ref ID J:46640)
    • 100% embryonic lethal in a pure 129S/SvEv background   (MGI Ref ID J:46640)

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

Ece1tm1Reh/Ece1tm1Reh

        involves: 129S6/SvEvTac * C57BL/6
  • mortality/aging
  • complete neonatal lethality
    • those mutants that do survive to term die within 30 minutes of birth   (MGI Ref ID J:46640)
  • partial embryonic lethality during organogenesis
    • 75% embryonic lethal in a C57BL/6-129/SvEv hybrid background 75% embryonic lethal in a C57BL/6-129/SvEv hybrid background   (MGI Ref ID J:46640)
    • most embryos die before E13.5   (MGI Ref ID J:46640)
  • pigmentation phenotype
  • abnormal choroid pigmentation
    • the neural crest derived melanocytes of the choroid and Harderian gland are absent   (MGI Ref ID J:46640)
  • abnormal melanocyte morphology
    • there are no detectable melanocytes in the dorsal skin of term mutants   (MGI Ref ID J:46640)
  • cardiovascular system phenotype
  • abnormal artery morphology
    • the peripheral vessels are congested and dilated   (MGI Ref ID J:46640)
    • absent right subclavian artery
      • the right subclavian artery is absent (7 out of 31)   (MGI Ref ID J:46640)
    • interrupted aortic arch
      • interruption of the aortic arch is observed at birth (18 out of 31)   (MGI Ref ID J:46640)
  • abnormal vasodilation
    • peripheral vascular dilation is seen in premorbid embryos   (MGI Ref ID J:46640)
  • decreased atrioventricular cushion size
    • the endocardial cushions are poorly developed   (MGI Ref ID J:46640)
  • double outlet right ventricle
    • the aorta arises from the right ventricle resulting in double outlet right ventricle (3 out of 10)   (MGI Ref ID J:46640)
  • enlarged heart
    • the atria are congested and dilated   (MGI Ref ID J:46640)
  • overriding aortic valve
    • the aorta overrides the crest of the ventricular septum in 5 out 10 pups   (MGI Ref ID J:46640)
  • pericardial effusion
    • along with dilation of the peripheral vasculature this is consistent with cardiac failure   (MGI Ref ID J:46640)
  • ventricular septal defect
    • ventricular septal defects are found in 100% (10 out of 10) of mutant embryos at birth   (MGI Ref ID J:46640)
  • craniofacial phenotype
  • abnormal squamosal bone morphology
    • the squamosal bone is hypoplastic and deformed   (MGI Ref ID J:46640)
  • abnormal styloid process morphology
    • the styloid process is severely deformed   (MGI Ref ID J:46640)
  • absent Meckel's cartilage
    • at birth Meckel's cartilage is absent   (MGI Ref ID J:46640)
  • absent external auditory canal
    • the external auditory meatus is absent   (MGI Ref ID J:46640)
  • absent incus   (MGI Ref ID J:46640)
  • absent malleus   (MGI Ref ID J:46640)
  • absent middle ear ossicles   (MGI Ref ID J:46640)
  • absent stapes
    • the cartilaginous rudiment of the stapes is absent in 11 out of 14 embryos   (MGI Ref ID J:46640)
  • absent tongue
    • at birth most of the tongue is absent   (MGI Ref ID J:46640)
  • alisphenoid bone hypoplasia
    • the alisphenoid cone is hypoplastic and deformed   (MGI Ref ID J:46640)
  • mandible hypoplasia
    • at birth the mandible is markedly reduced in size   (MGI Ref ID J:46640)
    • the teeth are normal however the lower incisors are embedded in loose mesenchyme rather than the mandible   (MGI Ref ID J:46640)
  • palatine bone hypoplasia
    • the palatine bone is hypoplastic and deformed   (MGI Ref ID J:46640)
  • endocrine/exocrine gland phenotype
  • absent salivary gland
    • at birth many of the submandibular and sublingual ducts are missing   (MGI Ref ID J:46640)
  • parathyroid hypoplasia
    • the parathyroid glands are hypoplastic   (MGI Ref ID J:46640)
  • small thyroid gland   (MGI Ref ID J:46640)
  • hearing/vestibular/ear phenotype
  • absent external auditory canal
    • the external auditory meatus is absent   (MGI Ref ID J:46640)
  • absent incus   (MGI Ref ID J:46640)
  • absent malleus   (MGI Ref ID J:46640)
  • absent middle ear ossicles   (MGI Ref ID J:46640)
  • absent stapes
    • the cartilaginous rudiment of the stapes is absent in 11 out of 14 embryos   (MGI Ref ID J:46640)
  • absent tympanic ring
    • the tympanic ring is absent   (MGI Ref ID J:46640)
  • homeostasis/metabolism phenotype
  • hydrops fetalis
    • generalized edema is seen in premorbid embryos   (MGI Ref ID J:46640)
  • pericardial effusion
    • along with dilation of the peripheral vasculature this is consistent with cardiac failure   (MGI Ref ID J:46640)
  • immune system phenotype
  • abnormal thymus morphology
    • the thymus does not fully descend into the thoracic cavity   (MGI Ref ID J:46640)
  • muscle phenotype
  • abnormal vasodilation
    • peripheral vascular dilation is seen in premorbid embryos   (MGI Ref ID J:46640)
  • skeleton phenotype
  • abnormal skeleton morphology
    • the ventral neck is sunken   (MGI Ref ID J:46640)
    • at birth fusion of the hyoid bone, thyroid cartilage and the basiphenoid bone, is seen resulting in a narrower airway   (MGI Ref ID J:46640)
    • abnormal squamosal bone morphology
      • the squamosal bone is hypoplastic and deformed   (MGI Ref ID J:46640)
    • abnormal styloid process morphology
      • the styloid process is severely deformed   (MGI Ref ID J:46640)
    • absent Meckel's cartilage
      • at birth Meckel's cartilage is absent   (MGI Ref ID J:46640)
    • absent incus   (MGI Ref ID J:46640)
    • absent malleus   (MGI Ref ID J:46640)
    • absent middle ear ossicles   (MGI Ref ID J:46640)
    • absent stapes
      • the cartilaginous rudiment of the stapes is absent in 11 out of 14 embryos   (MGI Ref ID J:46640)
    • alisphenoid bone hypoplasia
      • the alisphenoid cone is hypoplastic and deformed   (MGI Ref ID J:46640)
    • mandible hypoplasia
      • at birth the mandible is markedly reduced in size   (MGI Ref ID J:46640)
      • the teeth are normal however the lower incisors are embedded in loose mesenchyme rather than the mandible   (MGI Ref ID J:46640)
    • palatine bone hypoplasia
      • the palatine bone is hypoplastic and deformed   (MGI Ref ID J:46640)
  • vision/eye phenotype
  • abnormal choroid pigmentation
    • the neural crest derived melanocytes of the choroid and Harderian gland are absent   (MGI Ref ID J:46640)
  • nervous system phenotype
  • absent enteric neurons
    • enteric neurons are missing from the rectum of mutants at birth   (MGI Ref ID J:46640)
    • at E12.0 enteric neurons are seen only in the proximal gut and are absent beyond the ileocecal junction   (MGI Ref ID J:46640)
  • digestive/alimentary phenotype
  • absent salivary gland
    • at birth many of the submandibular and sublingual ducts are missing   (MGI Ref ID J:46640)
  • absent tongue
    • at birth most of the tongue is absent   (MGI Ref ID J:46640)
  • hematopoietic system phenotype
  • abnormal thymus morphology
    • the thymus does not fully descend into the thoracic cavity   (MGI Ref ID J:46640)

Ece1tm1Reh/Ece1tm1Reh

        involves: 129S6/SvEvTac * C57BL/6 * CBA
  • cardiovascular system phenotype
  • abnormal artery morphology
    • the branchial arch artery patterning abnormalities result in various types of great vessel malformations   (MGI Ref ID J:48566)
    • aberrant origin of the right subclavian artery
      • the right subclavian artery is missing or has a cervical origin in term embryos as a result of abnormal regression of right arch artery 4   (MGI Ref ID J:48566)
      • in term embryos with abnormal regression of right arch artery 4 and normal regression of the right ductus caroticus, the right dorsal aorta persists and the right subclavian artery is missing or originates from the dorsal aorta   (MGI Ref ID J:48566)
    • abnormal ascending aorta morphology
      • at E13.0 some embryos have extra branches from the ascending aorta   (MGI Ref ID J:48566)
    • abnormal fourth branchial arch artery morphology
      • in E11.5 embryos 75% (6/8) show enlargement of right arch artery 3 and relative narrowing of arch arteries 4 and 6   (MGI Ref ID J:48566)
      • this occurred more frequently on the right side (6 out of 8 than on the left 3 out of 8)   (MGI Ref ID J:48566)
      • at E12.0 - 12.5 and E13.0 - 13.5 right arch artery 4 shows signs of regression including decreased diameter and expression of a transgenic lacZ marker of arterial smooth muscle (11 out of 13 and 5 out of 7, respectively)   (MGI Ref ID J:48566)
      • at E12.0 - 12.5 and E13.0 - 13.5 regression of left arch artery 4 is also seen but not as frequently (7 out of 13 and 4 out of 7, respectively)   (MGI Ref ID J:48566)
      • between E11.5 and E13.5 the fourth arch arteries are diminished   (MGI Ref ID J:48566)
    • abnormal sixth branchial arch artery morphology
      • in E11.5 embryos 75% (6/8) show enlargement of right arch artery 3 and relative narrowing of arch arteries 4 and 6   (MGI Ref ID J:48566)
      • this occurred more frequently on the right side (6 out of 8 than on the left 3 out of 8)   (MGI Ref ID J:48566)
      • at E12.0 - 12.5 in 6 out of 13 embryos right arch artery 6 abnormally persists   (MGI Ref ID J:48566)
      • at E13.0 in embryos where the right arch artery 4 regressed the right arch artery 6 persisted   (MGI Ref ID J:48566)
    • abnormal third branchial arch artery morphology
      • in E11.5 embryos 75% (6/8) show enlargement of right arch artery 3 and relative narrowing of arch arteries 4 and 6   (MGI Ref ID J:48566)
      • this occurred more frequently on the right side (6 out of 8 than on the left 3 out of 8)   (MGI Ref ID J:48566)
      • at E12.0 - 12.5 right arch artery 3 is markedly enlarged in 6 out of 13 embryos   (MGI Ref ID J:48566)
      • at E12.5 arch arteries 3 become the dominant vessels bilaterally, accepting blood from the outflow tract   (MGI Ref ID J:48566)
      • at E12.5 the overall growth of arch arteries 3 toward the cranial direction is delayed and the external carotid fails to branch off of arch arteries 3   (MGI Ref ID J:48566)
    • double aortic arch
      • double aortic arch is found in term embryos when both the right and left arch arteries 4 abnormally regress or when left arch artery 6 abnormally regresses   (MGI Ref ID J:48566)
    • persistent ductus caroticus
      • at E12.5 in approximately 50% of embryos both right and left ductus caroticus remain   (MGI Ref ID J:48566)
    • persistent right dorsal aorta
      • at E12.0 - 12.5 and E13.0 - 13.5 the right dorsal aorta remains (6 out of 13 and 6 out of 7)   (MGI Ref ID J:48566)
      • at E13.0 the connection of the right dorsal aorta to the abdominal dorsal aorta persists   (MGI Ref ID J:48566)
      • in 2 of these embryos right sided dorsal aorta is observed where left arch arteries 4 and 6 and right arch artery 4 regress, while right arch artery 6 and the right dorsal aorta persist and form the major outflow tract from the heart   (MGI Ref ID J:48566)
  • double outlet right ventricle   (MGI Ref ID J:48566)
  • overriding aortic valve
    • other outflow tract abnormalities such as overriding aorta, double outlet right ventricle, and persistent truncus arteriosus are observed   (MGI Ref ID J:48566)
  • persistent truncus arteriosis   (MGI Ref ID J:48566)
  • craniofacial phenotype
  • abnormal fourth branchial arch artery morphology
    • in E11.5 embryos 75% (6/8) show enlargement of right arch artery 3 and relative narrowing of arch arteries 4 and 6   (MGI Ref ID J:48566)
    • this occurred more frequently on the right side (6 out of 8 than on the left 3 out of 8)   (MGI Ref ID J:48566)
    • at E12.0 - 12.5 and E13.0 - 13.5 right arch artery 4 shows signs of regression including decreased diameter and expression of a transgenic lacZ marker of arterial smooth muscle (11 out of 13 and 5 out of 7, respectively)   (MGI Ref ID J:48566)
    • at E12.0 - 12.5 and E13.0 - 13.5 regression of left arch artery 4 is also seen but not as frequently (7 out of 13 and 4 out of 7, respectively)   (MGI Ref ID J:48566)
    • between E11.5 and E13.5 the fourth arch arteries are diminished   (MGI Ref ID J:48566)
  • abnormal sixth branchial arch artery morphology
    • in E11.5 embryos 75% (6/8) show enlargement of right arch artery 3 and relative narrowing of arch arteries 4 and 6   (MGI Ref ID J:48566)
    • this occurred more frequently on the right side (6 out of 8 than on the left 3 out of 8)   (MGI Ref ID J:48566)
    • at E12.0 - 12.5 in 6 out of 13 embryos right arch artery 6 abnormally persists   (MGI Ref ID J:48566)
    • at E13.0 in embryos where the right arch artery 4 regressed the right arch artery 6 persisted   (MGI Ref ID J:48566)
  • abnormal third branchial arch artery morphology
    • in E11.5 embryos 75% (6/8) show enlargement of right arch artery 3 and relative narrowing of arch arteries 4 and 6   (MGI Ref ID J:48566)
    • this occurred more frequently on the right side (6 out of 8 than on the left 3 out of 8)   (MGI Ref ID J:48566)
    • at E12.0 - 12.5 right arch artery 3 is markedly enlarged in 6 out of 13 embryos   (MGI Ref ID J:48566)
    • at E12.5 arch arteries 3 become the dominant vessels bilaterally, accepting blood from the outflow tract   (MGI Ref ID J:48566)
    • at E12.5 the overall growth of arch arteries 3 toward the cranial direction is delayed and the external carotid fails to branch off of arch arteries 3   (MGI Ref ID J:48566)
  • embryogenesis phenotype
  • abnormal fourth branchial arch artery morphology
    • in E11.5 embryos 75% (6/8) show enlargement of right arch artery 3 and relative narrowing of arch arteries 4 and 6   (MGI Ref ID J:48566)
    • this occurred more frequently on the right side (6 out of 8 than on the left 3 out of 8)   (MGI Ref ID J:48566)
    • at E12.0 - 12.5 and E13.0 - 13.5 right arch artery 4 shows signs of regression including decreased diameter and expression of a transgenic lacZ marker of arterial smooth muscle (11 out of 13 and 5 out of 7, respectively)   (MGI Ref ID J:48566)
    • at E12.0 - 12.5 and E13.0 - 13.5 regression of left arch artery 4 is also seen but not as frequently (7 out of 13 and 4 out of 7, respectively)   (MGI Ref ID J:48566)
    • between E11.5 and E13.5 the fourth arch arteries are diminished   (MGI Ref ID J:48566)
  • abnormal sixth branchial arch artery morphology
    • in E11.5 embryos 75% (6/8) show enlargement of right arch artery 3 and relative narrowing of arch arteries 4 and 6   (MGI Ref ID J:48566)
    • this occurred more frequently on the right side (6 out of 8 than on the left 3 out of 8)   (MGI Ref ID J:48566)
    • at E12.0 - 12.5 in 6 out of 13 embryos right arch artery 6 abnormally persists   (MGI Ref ID J:48566)
    • at E13.0 in embryos where the right arch artery 4 regressed the right arch artery 6 persisted   (MGI Ref ID J:48566)
  • abnormal third branchial arch artery morphology
    • in E11.5 embryos 75% (6/8) show enlargement of right arch artery 3 and relative narrowing of arch arteries 4 and 6   (MGI Ref ID J:48566)
    • this occurred more frequently on the right side (6 out of 8 than on the left 3 out of 8)   (MGI Ref ID J:48566)
    • at E12.0 - 12.5 right arch artery 3 is markedly enlarged in 6 out of 13 embryos   (MGI Ref ID J:48566)
    • at E12.5 arch arteries 3 become the dominant vessels bilaterally, accepting blood from the outflow tract   (MGI Ref ID J:48566)
    • at E12.5 the overall growth of arch arteries 3 toward the cranial direction is delayed and the external carotid fails to branch off of arch arteries 3   (MGI Ref ID J:48566)

Ece1tm1Reh/Ece1tm1Reh

        involves: 129S6/SvEvTac * C57BL/6J
  • cardiovascular system phenotype
  • abnormal heart and great artery attachment
    • malalignment of great vessels and ventricles; the alignment between aortic and pulmonary vessel outflows remains in a spiral position as in wild-type, but the aortic valve and outflow shift rostrally and to the right so that the two valves appear in the same plane   (MGI Ref ID J:62261)
    • double outlet right ventricle
      • seen in a few mutants   (MGI Ref ID J:62261)
    • overriding aortic valve
      • seen in many mutants   (MGI Ref ID J:62261)
    • persistent truncus arteriosis
      • seen in one of ten mutants   (MGI Ref ID J:62261)
  • perimembraneous ventricular septal defect
    • most mutants show perimembranous ventricular septal defect   (MGI Ref ID J:62261)
View Research Applications

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

Developmental Biology Research
Craniofacial and Palate Defects
Embryonic Lethality (Homozygous)
Internal/Organ Defects
      heart
      heart: vasculature

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Ece1tm1Reh
Allele Name targeted mutation 1, Robert E Hammer
Allele Type Targeted (knock-out)
Common Name(s) ECE-1 -;
Mutation Made ByDr. Masashi Yanagisawa,   Southwestern Medical School
Strain of Origin129S6/SvEvTac
ES Cell Line NameSM1
ES Cell Line Strain129S6/SvEvTac
Gene Symbol and Name Ece1, endothelin converting enzyme 1
Chromosome 4
Gene Common Name(s) AW322500; ECE; expressed sequence AW322500;
Molecular Note A neomycin selection cassette replaced an exon containing coding sequences upstream of the zinc-binding motif. Western blot analysis on membrane preparations of homozygous E17-19 embryos confirmed that no detectable encoded protein was produced from this allele. [MGI Ref ID J:46640]

Genotyping

Genotyping Information


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Yanagisawa H; Yanagisawa M; Kapur RP; Richardson JA; Williams SC; Clouthier DE; de Wit D; Emoto N; Hammer RE. 1998. Dual genetic pathways of endothelin-mediated intercellular signaling revealed by targeted disruption of endothelin converting enzyme-1 gene. Development 125(5):825-36. [PubMed: 9449665]  [MGI Ref ID J:46640]

Additional References

Ece1tm1Reh related

Eckman EA; Adams SK; Troendle FJ; Stodola BA; Kahn MA; Fauq AH; Xiao HD; Bernstein KE; Eckman CB. 2006. Regulation of steady-state beta-amyloid levels in the brain by neprilysin and endothelin-converting enzyme but not angiotensin-converting enzyme. J Biol Chem 281(41):30471-8. [PubMed: 16912050]  [MGI Ref ID J:117188]

Eckman EA; Watson M; Marlow L; Sambamurti K; Eckman CB. 2003. Alzheimer's disease beta-amyloid peptide is increased in mice deficient in endothelin-converting enzyme. J Biol Chem 278(4):2081-4. [PubMed: 12464614]  [MGI Ref ID J:124414]

Gruber PJ; Epstein JA. 2004. Development gone awry: congenital heart disease. Circ Res 94(3):273-83. [PubMed: 14976138]  [MGI Ref ID J:96661]

Kuwaki T; Ling GY; Onodera M; Ishii T; Nakamura A; Ju KH; Cao WH; Kumada M; Kurihara H; Kurihara Y; Yazaki Y; Ohuchi T; Yanagisawa M; Fukuda Y. 1999. Endothelin in the central control of cardiovascular and respiratory functions. Clin Exp Pharmacol Physiol 26(12):989-94. [PubMed: 10626068]  [MGI Ref ID J:60070]

Morishima M; Yanagisawa H; Yanagisawa M; Baldini A. 2003. Ece1 and Tbx1 define distinct pathways to aortic arch morphogenesis. Dev Dyn 228(1):95-104. [PubMed: 12950083]  [MGI Ref ID J:85487]

Renolleau S; Dauger S; Vardon G; Levacher B; Simonneau M; Yanagisawa M; Gaultier C; Gallego J. 2001. Impaired ventilatory responses to hypoxia in mice deficient in endothelin-converting-enzyme-1. Pediatr Res 49(5):705-12. [PubMed: 11328956]  [MGI Ref ID J:102275]

Yanagisawa H; Hammer RE; Richardson JA; Emoto N; Williams SC; Takeda Si; Clouthier DE; Yanagisawa M. 2000. Disruption of ECE-1 and ECE-2 reveals a role for endothelin-converting enzyme-2 in murine cardiac development. J Clin Invest 105(10):1373-82. [PubMed: 10811845]  [MGI Ref ID J:62261]

Yanagisawa H; Hammer RE; Richardson JA; Williams SC; Clouthier DE; Yanagisawa M. 1998. Role of Endothelin-1/Endothelin-A receptor-mediated signaling pathway in the aortic arch patterning in mice [see comments] J Clin Invest 102(1):22-33. [PubMed: 9649553]  [MGI Ref ID J:48566]

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 maintained as a live colony, heterozygotes may be bred. Homozygotes die before embryonic day 13.5 (E13.5) on a 129 genetic background. On a mixed 129-C57BL/6 background, lethality is approximately 75%, but pups die shortly after birth due to impaired breathing.

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.

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The Jackson Laboratory's Genotype Promise

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

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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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