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- Description
- Disease & phenotype
- Genes & alleles
- Genotyping
- Health & care
- References
- Pricing & purchasing
- Terms of use
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 Congenic; Mutant Strain; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Species laboratory mouse Generation N3+2F1PN1
Generation DefinitionsDonating Investigator David J Anderson, California Institute of Technology, HHMI Description
Mice homozygous for this targeted mutation show growth retardation and enlargement of the heart at embryonic day 10 (E10), with 100% lethality occurring around E11. Reporter protein expression patterns are consistent with arterial, but not venous, expression of the endogenous gene; prominent lacZ signal is observed in hindbrain and somites, with lower levels in aorta and heart as early as E8.25. Expression in the yolk sac was first detected at E8.5, and is also observed in nephrogenic mesoderm and branchial arches. Homozygous embryos show defective angiogenic remodeling at the capillary plexus stage in both yolk sac and head. Endothelial vessel support cell differentiation of the yolk sac is also defective. Homozygotes lack myocardial trabecular extensions, and capillary ingrowth into the neural tube does not occur. Heterozygous mice are viable, fertile, exhibit no behavioral defects, and have identical lacZ expression patterns. These mutant mice may be useful in studying the cellular and molecular mechanisms underlying vasculogenesis and angiogenesis, the topography of neovascularization, and adult neovascularization, including tumor angiogenesis.The developmental abnormalities in homozygous mice closely resemble those observed for mutant mice bearing a lacZ-expressing null mutation of the ephrin B2 receptor (see Stock No. 006044 Ephb4tm1And).
Development
A targeting vector was designed with a tau-lacZ coding sequence immediately followed by a PGKneo gene. This sequence was inserted in-frame after the translational start ATG and replaced the latter portion of exon 1 of the endogenous gene. The construct was microinjected into 129S7/SvEvBrd-derived AB1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into blastocysts and the resulting chimeric males were bred to C57BL/6 females. Heterozygous mice were bred to C57BL/6 for at least 3 generations before arriving at The Jackson Laboratory. Upon arrival, heterozygotes were bred with C57BL/6J for more than two generations.
Control Information
| Control | ||
|---|---|---|
| Wild-type from the colony | ||
| 000664 C57BL/6J | ||
| Considerations for Choosing Controls | ||
Related Strains
lacZ Expression Strains
View lacZ Expression Strains (256 strains)
006042 B6.129S7-Efnb2tm2And/J 007843 B6;129S4-Efnb2tm2Sor/J
Additional Web Information
Fluorescent Proteins/lacZ Systems
Phenotype
Phenotype Information
assigned by genotype
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Efnb2tm1And/Efnb2tm1And
involves: 129S7/SvEvBrd
- mortality/aging
- complete embryonic lethality during organogenesis
- all homozygotes die by E11 (MGI Ref ID J:75288)
- embryogenesis phenotype
- abnormal vitelline vasculature morphology
- at E9.5, intercalation bidirectional growth of arteries and veins in the yolk sac is absent in mutants across the anterior-posterior compared to heterozygous controls (MGI Ref ID J:75288)
- defects in yolk sac angiogenesis are apparent at 9.0, becoming prominent at E9.5 (MGI Ref ID J:75288)
- in the anterior region of the yolk sac, there is a block to remodeling at the capillary plexus stage for arterial and venous vessels at E9-9.5 (MGI Ref ID J:75288)
- support cells in mutants are more rounded in appearance in contrast to the elongated support cells associated with the endothelial vessels in control heterozygotes at E10 and 10.5 (MGI Ref ID J:75288)
- in contrast to heterozygote yolk sacs, capillary diameter appears relatively uniform between E9.5 through E10.5 rather than increasing; mutant capillaries fail to delaminate from the basal endodermal layer (MGI Ref ID J:75288)
- embryonic growth retardation
- apparent by E10 (MGI Ref ID J:75288)
- growth/size phenotype
- embryonic growth retardation
- apparent by E10 (MGI Ref ID J:75288)
- cardiovascular system phenotype
- *normal* cardiovascular system phenotype
- abnormal angiogenesis
- embryonic angiogenesis is defective such that the capillary bed in the heads of mutant embryos appears dilated and apparently arrested at the primary plexus stage (MGI Ref ID J:75288)
- anterior-most branches of the internal carotid artery fail to develop (MGI Ref ID J:75288)
- capillary ingrowth into the neural tube fails to occur; endothelial cells remain associated with the surface of the developing spinal cord (MGI Ref ID J:75288)
- abnormal cardinal vein morphology
- anterior branches of the anterior cardinal vein form but are slightly dilated (MGI Ref ID J:75288)
- abnormal endocardium morphology
- abnormal heart ventricle morphology
- abnormal myocardium layer morphology
- marker analysis indicates that ventricular myocardial differentiation is impaired (MGI Ref ID J:119151)
- absent myocardial trabeculae
- at E10, myocardial trabecular extensions are absent (MGI Ref ID J:75288)
- abnormal vitelline vasculature morphology
- at E9.5, intercalation bidirectional growth of arteries and veins in the yolk sac is absent in mutants across the anterior-posterior compared to heterozygous controls (MGI Ref ID J:75288)
- defects in yolk sac angiogenesis are apparent at 9.0, becoming prominent at E9.5 (MGI Ref ID J:75288)
- in the anterior region of the yolk sac, there is a block to remodeling at the capillary plexus stage for arterial and venous vessels at E9-9.5 (MGI Ref ID J:75288)
- support cells in mutants are more rounded in appearance in contrast to the elongated support cells associated with the endothelial vessels in control heterozygotes at E10 and 10.5 (MGI Ref ID J:75288)
- in contrast to heterozygote yolk sacs, capillary diameter appears relatively uniform between E9.5 through E10.5 rather than increasing; mutant capillaries fail to delaminate from the basal endodermal layer (MGI Ref ID J:75288)
- enlarged heart
- heart is enlarged in E10 embryos (MGI Ref ID J:75288)
- muscle phenotype
- absent myocardial trabeculae
- at E10, myocardial trabecular extensions are absent (MGI Ref ID J:75288)
Efnb2tm1And/Efnb2tm1And
involves: 129S7/SvEvBrd * C57BL/6
- cardiovascular system phenotype
- abnormal angiogenesis
- embryonic angiogenesis is defective such that the capillary bed in the heads of mutant embryos appears dilated and apparently arrested at the primary plexus stage (MGI Ref ID J:74909)
- capillary ingrowth into the neural tube fails to occur; endothelial cells remain associated with the surface of the developing spinal cord (MGI Ref ID J:74909)
- anterior-most branches of the internal carotid artery fail to develop (MGI Ref ID J:74909)
- abnormal anterior cardinal vein morphology
- embryos show a failure of anterior cardinal vein assembly, resulting in a plexus of disorganized small-diameter vessels (MGI Ref ID J:74909)
- abnormal developmental vascular remodeling
- embryos fail to undergo angiogenic remodeling of the intersomitic vasculature (MGI Ref ID J:74909)
- abnormal heart looping
- heart looping defects (MGI Ref ID J:74909)
- abnormal vitelline vasculature morphology (MGI Ref ID J:74909)
- absent myocardial trabeculae (MGI Ref ID J:74909)
- enlarged heart (MGI Ref ID J:74909)
- embryogenesis phenotype
- abnormal vitelline vasculature morphology (MGI Ref ID J:74909)
- decreased embryo size (MGI Ref ID J:74909)
- growth/size phenotype
- decreased embryo size (MGI Ref ID J:74909)
- muscle phenotype
- absent myocardial trabeculae (MGI Ref ID J:74909)
This mouse can be used to support research in many areas including:
Cardiovascular Research
Vascular Defects
Developmental Biology Research
Embryonic Lethality (Homozygous)
Internal/Organ Defects
heart
heart: vasculature
vasculature
Research Tools
lacZ Expression
Cancer Research
endothelial cell marker for neovascularization
Cardiovascular Research
endothelial cell marker (lacZ) for neovascularization
endothelial cell marker for neovascularization
Developmental Biology Research
Genetics Research
Tissue/Cell Markers
Tissue/Cell Markers: endothelial cell markers for neovascularization
Tissue/Cell Markers: endothelial cells
Genes & Alleles
Gene & Allele Information provided by MGI
| Allele Symbol | Efnb2tm1And | ||
|---|---|---|---|
| Allele Name | targeted mutation 1, David J Anderson | ||
| Allele Type | Targeted (Reporter) | ||
| Common Name(s) | EphrinB2LacZ; EphrinB2tlacz; ephrin-B2taulacZ; ephrin-B2tlacZ; | ||
| Mutation Made By | David Anderson, California Institute of Technology, HHMI | ||
| Strain of Origin | 129S7/SvEvBrd-Hprt<+> | ||
| ES Cell Line Name | AB1 | ||
| ES Cell Line Strain | 129S7/SvEvBrd-Hprt<+> | ||
| Site of Expression | lacZ expression is detected in hindbrain and somites, with lower levels detected in aorta and heart at embryonic day 8.25 (E8.25). Expression is detected in the yolk sac at E8.5 and is also detected in nephrogenic mesoderm and branchial arches. | ||
| Expressed Gene | lacZ, beta-galactosidase, E. coli | ||
| Molecular Note | The targeting strategy involved deleting the signal sequence and fusing a tau-lacZ PGK-neomycin cassette in frame with the initiation codon. There was no expression of endogenous mRNA by in situ hybridization in homozygous mutant animals. Heterozygous embryos expressed beta-galactosidase in a pattern that was indistinguishable from the endogenous expression pattern. [MGI Ref ID J:75288] | ||
| Gene Symbol and Name | Efnb2, ephrin B2 | ||
| Chromosome | 8 | ||
| Gene Common Name(s) | ELF-2; EPLG5; Epl5; HTKL; Htk-L; LERK-5; LERK5; NLERK-1; eph-related receptor tyrosine kinase ligand 5; | ||
Genotyping
Genotyping Information
Genotyping Protocols
Efnb2tm1And, Separated PCR
Helpful Links
Genotyping resources and troubleshooting
References
References provided by MGI
Selected Reference(s)
Wang HU; Chen ZF; Anderson DJ. 1998. Molecular distinction and angiogenic interaction between embryonic arteries and veins revealed by ephrin-B2 and its receptor Eph-B4. Cell 93(5):741-53. [PubMed: 9630219] [MGI Ref ID J:75288]
Additional References
Efnb2tm1And relatedBoulday G; Rudini N; Maddaluno L; Blecon A; Arnould M; Gaudric A; Chapon F; Adams RH; Dejana E; Tournier-Lasserve E. 2011. Developmental timing of CCM2 loss influences cerebral cavernous malformations in mice. J Exp Med 208(9):1835-47. [PubMed: 21859843] [MGI Ref ID J:177584]
Corada M; Nyqvist D; Orsenigo F; Caprini A; Giampietro C; Taketo MM; Iruela-Arispe ML; Adams RH; Dejana E. 2010. The Wnt/beta-catenin pathway modulates vascular remodeling and specification by upregulating Dll4/Notch signaling. Dev Cell 18(6):938-49. [PubMed: 20627076] [MGI Ref ID J:163848]
Davis RB; Curtis CD; Griffin CT. 2013. BRG1 promotes COUP-TFII expression and venous specification during embryonic vascular development. Development 140(6):1272-81. [PubMed: 23406903] [MGI Ref ID J:194470]
Egawa G; Osawa M; Uemura A; Miyachi Y; Nishikawa S. 2009. Transient expression of ephrin b2 in perinatal skin is required for maintenance of keratinocyte homeostasis. J Invest Dermatol 129(10):2386-95. [PubMed: 19571816] [MGI Ref ID J:157054]
Gerety SS; Anderson DJ. 2002. Cardiovascular ephrinB2 function is essential for embryonic angiogenesis. Development 129(6):1397-410. [PubMed: 11880349] [MGI Ref ID J:74909]
Grego-Bessa J; Luna-Zurita L; del Monte G; Bolos V; Melgar P; Arandilla A; Garratt AN; Zang H; Mukouyama YS; Chen H; Shou W; Ballestar E; Esteller M; Rojas A; Perez-Pomares JM; de la Pompa JL. 2007. Notch signaling is essential for ventricular chamber development. Dev Cell 12(3):415-29. [PubMed: 17336907] [MGI Ref ID J:119151]
Hayashi S; Asahara T; Masuda H; Isner JM; Losordo DW. 2005. Functional ephrin-B2 expression for promotive interaction between arterial and venous vessels in postnatal neovascularization. Circulation 111(17):2210-8. [PubMed: 15851594] [MGI Ref ID J:109693]
Kim YH; Hu H; Guevara-Gallardo S; Lam MT; Fong SY; Wang RA. 2008. Artery and vein size is balanced by Notch and ephrin B2/EphB4 during angiogenesis. Development 135(22):3755-64. [PubMed: 18952909] [MGI Ref ID J:144857]
Krebs LT; Shutter JR; Tanigaki K; Honjo T; Stark KL; Gridley T. 2004. Haploinsufficient lethality and formation of arteriovenous malformations in Notch pathway mutants. Genes Dev 18(20):2469-73. [PubMed: 15466160] [MGI Ref ID J:93125]
Krebs LT; Starling C; Chervonsky AV; Gridley T. 2010. Notch1 activation in mice causes arteriovenous malformations phenocopied by ephrinB2 and EphB4 mutants. Genesis 48(3):146-50. [PubMed: 20101599] [MGI Ref ID J:163061]
Lavine KJ; Kovacs A; Ornitz DM. 2008. Hedgehog signaling is critical for maintenance of the adult coronary vasculature in mice. J Clin Invest 118(7):2404-14. [PubMed: 18568073] [MGI Ref ID J:137685]
Lavine KJ; Long F; Choi K; Smith C; Ornitz DM. 2008. Hedgehog signaling to distinct cell types differentially regulates coronary artery and vein development. Development 135(18):3161-71. [PubMed: 18725519] [MGI Ref ID J:138814]
Li W; Kohara H; Uchida Y; James JM; Soneji K; Cronshaw DG; Zou YR; Nagasawa T; Mukouyama YS. 2013. Peripheral nerve-derived CXCL12 and VEGF-A regulate the patterning of arterial vessel branching in developing limb skin. Dev Cell 24(4):359-71. [PubMed: 23395391] [MGI Ref ID J:195048]
Mallory BP; Mead TJ; Wiginton DA; Kulkarni RM; Greenberg JM; Akeson AL. 2006. Lymphangiogenesis in the developing lung promoted by VEGF-A. Microvasc Res 72(1-2):62-73. [PubMed: 16806288] [MGI Ref ID J:129289]
Murphy PA; Kim TN; Lu G; Bollen AW; Schaffer CB; Wang RA. 2012. Notch4 normalization reduces blood vessel size in arteriovenous malformations. Sci Transl Med 4(117):117ra8. [PubMed: 22261032] [MGI Ref ID J:183703]
Nam J; Onitsuka I; Hatch J; Uchida Y; Ray S; Huang S; Li W; Zang H; Ruiz-Lozano P; Mukouyama YS. 2013. Coronary veins determine the pattern of sympathetic innervation in the developing heart. Development 140(7):1475-85. [PubMed: 23462468] [MGI Ref ID J:194919]
Sorensen LK; Brooke BS; Li DY; Urness LD. 2003. Loss of distinct arterial and venous boundaries in mice lacking endoglin, a vascular-specific TGFbeta coreceptor. Dev Biol 261(1):235-50. [PubMed: 12941632] [MGI Ref ID J:85366]
Wallgard E; Nitzsche A; Larsson J; Guo X; Dieterich LC; Dimberg A; Olofsson T; Ponten FC; Makinen T; Kalen M; Hellstrom M. 2012. Paladin (X99384) is expressed in the vasculature and shifts from endothelial to vascular smooth muscle cells during mouse development. Dev Dyn 241(4):770-86. [PubMed: 22354871] [MGI Ref ID J:181634]
Zindl CL; Kim TH; Zeng M; Archambault AS; Grayson MH; Choi K; Schreiber RD; Chaplin DD. 2009. The lymphotoxin LTalpha(1)beta(2) controls postnatal and adult spleen marginal sinus vascular structure and function. Immunity 30(3):408-20. [PubMed: 19303389] [MGI Ref ID J:147033]
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 & Husbandry When maintaining a live colony, these mice are bred as heterozygotes. Homozygous mice die in utero.
Pricing and Purchasing
Pricing, Supply Level & Notes, Controls
| Pricing for USA, Canada and Mexico shipping destinations |
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Cryopreserved
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $2085.00 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 |
|
Cryopreserved
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $2710.50 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).
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Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.
General Supply Notes
- Genomic DNA is available for this strain from the Mouse DNA Resource.
Control Information
| Control | ||
|---|---|---|
| Wild-type from the colony | ||
| 000664 C57BL/6J | ||
| Considerations for Choosing Controls | ||
| Control Pricing Information for Genetically Engineered Mutant Strains. | ||
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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.Ordering Information
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For Licensing and Use Restrictions view the link(s) below:
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