Strain Name:

B6.129-Dll1tm1Gos/J

Stock Number:

002957

Order this mouse

Availability:

Cryopreserved - Ready for recovery

Other products are available, see Purchasing Information for Cryopreserved Embryos

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.
Specieslaboratory mouse
Background Strain C57BL/6J
Donor Strain 129X1 x 129S1 via R1 (+Kitl-SlJ) ES cell line
 
Donating InvestigatorDr. Achim Gossler,   Medizinische Hochschule Hannover

Description
Mouse embyros homozygous for the Dll1tm1Gos targeted mutation establish a primary metameric pattern in the mesoderm. Cytodifferentiation appears normal, but the segments have no cranio-caudal polarity, and no epithelial somites form. Caudal sclerotome halves do not condense, and the pattern of spinal ganglia and nerves is perturbed, indicating loss of segment polarity. Myoblasts span segment borders, demonstrating that these borders are not maintained.

Development
The replacement vector was constructed by inserting a 4-kilobase ClaI/XhoI fragment, which encodes a part of the beta-galactosidase gene followed by the PGK-neo cassette, and a 2.6-kb XhoI/EcoRI fragment as the 3' homologous region of the replacement vector into pKS+.

Control Information

  Control
   Wild-type from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

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

Dll1tm1Gos/Dll1+

        C3Fe.129-Dll1tm1Gos
  • immune system phenotype
  • decreased B-1 B cell number
    • in female mice   (MGI Ref ID J:150183)
  • decreased CD4-positive T cell number
    • in female, but not male, mice   (MGI Ref ID J:150183)
  • decreased CD8-positive T cell number
    • female mice exhibit a decrease in CD8alpha,beta T cells compared with wild-type mice   (MGI Ref ID J:150183)
  • decreased IgA level
    • in female mice   (MGI Ref ID J:150183)
  • decreased IgG1 level
    • in female mice   (MGI Ref ID J:150183)
  • decreased IgG2b level
    • in female mice   (MGI Ref ID J:150183)
  • decreased IgG3 level
    • in female mice   (MGI Ref ID J:150183)
  • increased B cell number
    • in female, but not male, mice   (MGI Ref ID J:150183)
  • increased CD8-positive T cell number
    • male mice exhibit an increase in CD8alpha,beta T cells compared with wild-type mice   (MGI Ref ID J:150183)
  • homeostasis/metabolism phenotype
  • abnormal basal metabolism
    • mice exhibit reduced metabolized energy compared with wild-type mice   (MGI Ref ID J:150183)
    • increased basal metabolism
      • when normalized to individual body weight, male mice congenic on a C3 background exhibit increased metabolized energy while male mice exhibit only a tendency compared with wild-type mice whereas on a 129 background only female mice exhibit increased metabolized energy compared with wild-type mice   (MGI Ref ID J:150183)
  • abnormal enzyme/coenzyme activity
    • alpha-amylase activity is decreased compared to in wild-type mice   (MGI Ref ID J:150183)
  • decreased blood uric acid level   (MGI Ref ID J:150183)
  • decreased circulating cholesterol level
  • decreased circulating total protein level   (MGI Ref ID J:150183)
  • decreased circulating triglyceride level   (MGI Ref ID J:150183)
  • skeleton phenotype
  • decreased bone mineral density
    • whole body bone mineral density is reduced compared to in wild-type mice   (MGI Ref ID J:150183)
    • whole body bone mineral content is reduced in female mice and tends to be reduced in male mice compared with wild-type mice   (MGI Ref ID J:150183)
    • however, bone content related to body weight is normal   (MGI Ref ID J:150183)
  • decreased lumbar vertebrae number
  • increased bone mineral density
    • specific bone mineral density is increased compared to in wild-type mice   (MGI Ref ID J:150183)
    • however, bone content related to body weight is normal   (MGI Ref ID J:150183)
  • growth/size/body phenotype
  • decreased body height
    • mice are shorter than wild-type mice   (MGI Ref ID J:150183)
  • decreased body weight
    • at 6 weeks, average body weight is decreased compared with wild-type mice   (MGI Ref ID J:150183)
    • average fat-free dry mass is reduced compared to in wild-type mice   (MGI Ref ID J:150183)
    • however, body weight normalized to energy uptake is normal   (MGI Ref ID J:150183)
  • decreased lean body mass
    • average body lean body mass and the average fat to lean mass ratio are reduced compared to in wild-type mice   (MGI Ref ID J:150183)
  • decreased total body fat amount
    • average body fat content and the average fat to lean mass ratio are reduced compared to in wild-type mice   (MGI Ref ID J:150183)
  • increased susceptibility to weight loss
    • mice fasted for 2 days exhibit a greater loss of body weight compared with similarly treated wild-type mice   (MGI Ref ID J:150183)
  • cardiovascular system phenotype
  • abnormal Q wave
    • the Q amplitude is increased compared to in wild-type mice   (MGI Ref ID J:150183)
  • decreased heart rate
    • pulse and heart rate in female mice are decreased compared to in wild-type mice   (MGI Ref ID J:150183)
  • increased mean systemic arterial blood pressure
    • at 14 weeks in male mice   (MGI Ref ID J:150183)
  • increased systemic arterial diastolic blood pressure
    • at 14 weeks in male mice   (MGI Ref ID J:150183)
  • increased systemic arterial systolic blood pressure
    • at 14 weeks in male mice   (MGI Ref ID J:150183)
  • adipose tissue phenotype
  • decreased total body fat amount
    • average body fat content and the average fat to lean mass ratio are reduced compared to in wild-type mice   (MGI Ref ID J:150183)
  • behavior/neurological phenotype
  • decreased food intake
    • mice consume less food and have a reduced energy uptake compared with wild-type mice   (MGI Ref ID J:150183)
  • hypoactivity
    • mice exhibit a tendency towards reduced locomotor activity compared with wild-type mice   (MGI Ref ID J:150183)
  • digestive/alimentary phenotype
  • abnormal defecation
    • mice produce less feces than wild-type mice   (MGI Ref ID J:150183)
  • hematopoietic system phenotype
  • decreased B-1 B cell number
    • in female mice   (MGI Ref ID J:150183)
  • decreased CD4-positive T cell number
    • in female, but not male, mice   (MGI Ref ID J:150183)
  • decreased CD8-positive T cell number
    • female mice exhibit a decrease in CD8alpha,beta T cells compared with wild-type mice   (MGI Ref ID J:150183)
  • decreased IgA level
    • in female mice   (MGI Ref ID J:150183)
  • decreased IgG1 level
    • in female mice   (MGI Ref ID J:150183)
  • decreased IgG2b level
    • in female mice   (MGI Ref ID J:150183)
  • decreased IgG3 level
    • in female mice   (MGI Ref ID J:150183)
  • increased B cell number
    • in female, but not male, mice   (MGI Ref ID J:150183)
  • increased CD8-positive T cell number
    • male mice exhibit an increase in CD8alpha,beta T cells compared with wild-type mice   (MGI Ref ID J:150183)

Dll1tm1Gos/Dll1+

        involves: 129S1/Sv * 129X1/SvJ
  • immune system phenotype
  • decreased CD4-positive T cell number
    • a non-significant reduction   (MGI Ref ID J:150183)
  • increased B cell number
    • in female but not male mice   (MGI Ref ID J:150183)
  • homeostasis/metabolism phenotype
  • increased basal metabolism
    • when normalized to individual body weight, female mice on a 129 background exhibit increased metabolized energy while male mice exhibit only a tendency compared with wild-type mice whereas on a congenic C3 background only male mice exhibit increased metabolized energy compared with wild-type mice   (MGI Ref ID J:150183)
  • growth/size/body phenotype
  • increased susceptibility to weight loss
    • mice fasted for 2 days exhibit a greater loss of body weight compared with similarly treated wild-type mice   (MGI Ref ID J:150183)
  • skeleton phenotype
  • abnormal bone mineral density
    • similar to on a C3 background, mice exhibit abnormal bone mineral density compared with wild-type mice   (MGI Ref ID J:150183)
  • hematopoietic system phenotype
  • decreased CD4-positive T cell number
    • a non-significant reduction   (MGI Ref ID J:150183)
  • increased B cell number
    • in female but not male mice   (MGI Ref ID J:150183)

Dll1tm1Gos/Dll1+

        Background Not Specified
  • growth/size/body phenotype
  • decreased body weight   (MGI Ref ID J:165965)
  • increased body weight   (MGI Ref ID J:165965)
  • hematopoietic system phenotype
  • increased leukocyte cell number   (MGI Ref ID J:165965)
    • increased lymphocyte cell number   (MGI Ref ID J:165965)
    • increased monocyte cell number   (MGI Ref ID J:165965)
  • immune system phenotype
  • increased leukocyte cell number   (MGI Ref ID J:165965)
    • increased lymphocyte cell number   (MGI Ref ID J:165965)
    • increased monocyte cell number   (MGI Ref ID J:165965)
  • other phenotype
  • other phenotype   (MGI Ref ID J:165965)

Dll1tm1Gos/Dll1tm1Gos

        involves: 129S1/Sv * 129X1/SvJ
  • mortality/aging
  • complete embryonic lethality during organogenesis
  • nervous system phenotype
  • abnormal neuron differentiation
    • overproduction of Isl1/Isl2+ motoneurons at E9.5 in the intermediate and ventral neural tube   (MGI Ref ID J:156172)
    • increase in the number of Chx10+ V2a, Gata3+ V2b and Evx1/Evx2+ V0 neurons at E10.5 in the intermediate and ventral neural tube   (MGI Ref ID J:156172)
    • expression analysis indicates and increase in the pace of neurogenesis   (MGI Ref ID J:156172)
    • decreased neuronal precursor cell number
      • about a 40 - 50% reduction in the number of progenitor cells in the p0 domain of the spinal cord at E10.5   (MGI Ref ID J:156172)
      • progressive depletion of motorneuron progenitors over time   (MGI Ref ID J:156172)
  • increased neuron number
    • increase in the number of Chx10+ V2a, Gata3+ V2b and Evx1/Evx2+ V0 neurons at E10.5 in the intermediate and ventral neural tube   (MGI Ref ID J:156172)
    • increased motor neuron number
      • overproduction of Isl1/Isl2+ motoneurons at E9.5 in the intermediate and ventral neural tube   (MGI Ref ID J:156172)
  • cellular phenotype
  • abnormal neuron differentiation
    • overproduction of Isl1/Isl2+ motoneurons at E9.5 in the intermediate and ventral neural tube   (MGI Ref ID J:156172)
    • increase in the number of Chx10+ V2a, Gata3+ V2b and Evx1/Evx2+ V0 neurons at E10.5 in the intermediate and ventral neural tube   (MGI Ref ID J:156172)
    • expression analysis indicates and increase in the pace of neurogenesis   (MGI Ref ID J:156172)
    • decreased neuronal precursor cell number
      • about a 40 - 50% reduction in the number of progenitor cells in the p0 domain of the spinal cord at E10.5   (MGI Ref ID J:156172)
      • progressive depletion of motorneuron progenitors over time   (MGI Ref ID J:156172)

Dll1tm1Gos/Dll1tm1Gos

        involves: 129S1/Sv * 129X1/SvJ * C57BL/6J
  • mortality/aging
  • complete embryonic lethality during organogenesis
    • death around E12   (MGI Ref ID J:39633)
  • embryogenesis phenotype
  • abnormal direction of embryo turning
    • tail rotation to the left in about 48% of embryos but random relative to heart looping   (MGI Ref ID J:80018)
  • abnormal notochord morphology
    • some regions appear as a sheet of cells associated with the dorsal primitive gut endoderm   (MGI Ref ID J:80018)
    • reduced number of notochord cells   (MGI Ref ID J:80018)
  • abnormal paraxial mesoderm morphology
    • severe patterning defects in paraxial mesoderm   (MGI Ref ID J:39633)
  • abnormal primitive node morphology
    • rupture of surface, bulging of cells   (MGI Ref ID J:80018)
    • by late headfold stage, abnormal cell morphology disrupts symmetry   (MGI Ref ID J:80018)
    • absent embryonic cilia
      • loss of monociliated cells   (MGI Ref ID J:80018)
  • abnormal somite development   (MGI Ref ID J:39633)
    • abnormal somite shape
      • irregularly shaped segments in the trunk   (MGI Ref ID J:39633)
      • distinct dermatomes present at E10,5 but segmental arrangement of myotome and sclerotome cells is disturbed   (MGI Ref ID J:39633)
      • myoblasts sometimes span space between adjacent segments   (MGI Ref ID J:39633)
    • incomplete somite formation
      • absence of segments in tail bud   (MGI Ref ID J:39633)
      • caudal sclerotome forms a uniform, loose, non segmental mass   (MGI Ref ID J:39633)
  • enlarged floor plate
    • enlarged floor plate between E8.5 and E10.5   (MGI Ref ID J:80018)
  • nervous system phenotype
  • abnormal brain development
    • hyperplastic CNS   (MGI Ref ID J:39633)
  • abnormal neuron differentiation
    • excessive neuronal differentiation in CNS   (MGI Ref ID J:39633)
  • abnormal somatic nervous system morphology   (MGI Ref ID J:39633)
    • abnormal spinal nerve morphology
      • wide   (MGI Ref ID J:39633)
      • irregularly spaced   (MGI Ref ID J:39633)
    • fused dorsal root ganglion   (MGI Ref ID J:39633)
  • enlarged floor plate
    • enlarged floor plate between E8.5 and E10.5   (MGI Ref ID J:80018)
  • cardiovascular system phenotype
  • abnormal direction of heart looping
    • heart looping to the left in about 50% of embryos   (MGI Ref ID J:80018)
    • looping is sometimes incomplete at E8.5-9.5   (MGI Ref ID J:80018)
  • hemorrhage
    • severely hemorrhagic after E10   (MGI Ref ID J:39633)
  • endocrine/exocrine gland phenotype
  • abnormal pancreas development
    • pancreatic bud decreased in size   (MGI Ref ID J:57072)
    • composed primarily of endocrine cells   (MGI Ref ID J:57072)
  • cellular phenotype
  • abnormal neuron differentiation
    • excessive neuronal differentiation in CNS   (MGI Ref ID J:39633)
View Research Applications

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

Dll1tm1Gos related

Developmental Biology Research
Embryonic Lethality (Homozygous)
Internal/Organ Defects
Neural Tube Defects
Neurodevelopmental Defects

Neurobiology Research
Neural Tube Defects
Neurodevelopmental Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Dll1tm1Gos
Allele Name targeted mutation 1, Achim Gossler
Allele Type Targeted (Reporter)
Common Name(s) Dll1-; Dll1lacZ;
Mutation Made ByDr. Achim Gossler,   Medizinische Hochschule Hannover
Strain of Origin(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
ES Cell Line NameR1
ES Cell Line Strain(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
Gene Symbol and Name Dll1, delta-like 1 (Drosophila)
Chromosome 17
Gene Common Name(s) DELTA1; DL1; Delta;
Molecular Note In-frame insertion of a LacZ-PGK-neomycin resistance cassette replaced sequences that code for amino acids 2-116 of the Dll1 gene. [MGI Ref ID J:39633]

Genotyping

Genotyping Information

Genotyping Protocols

Dll1tm1 Gos, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Hrabe de Angelis M; McIntyre J 2nd; Gossler A. 1997. Maintenance of somite borders in mice requires the Delta homologue DII1. Nature 386(6626):717-21. [PubMed: 9109488]  [MGI Ref ID J:39633]

Additional References

Kume T; Jiang H; Topczewska JM; Hogan BL. 2001. The murine winged helix transcription factors, Foxc1 and Foxc2, are both required for cardiovascular development and somitogenesis. Genes Dev 15(18):2470-82. [PubMed: 11562355]  [MGI Ref ID J:71693]

Zhang N; Norton CR; Gridley T. 2002. Segmentation defects of Notch pathway mutants and absence of a synergistic phenotype in lunatic fringe/radical fringe double mutant mice. Genesis 33(1):21-8. [PubMed: 12001066]  [MGI Ref ID J:77247]

Dll1tm1Gos related

Ahnfelt-Ronne J; Jorgensen MC; Klinck R; Jensen JN; Fuchtbauer EM; Deering T; Macdonald RJ; Wright CV; Madsen OD; Serup P. 2012. Ptf1a-mediated control of Dll1 reveals an alternative to the lateral inhibition mechanism. Development 139(1):33-45. [PubMed: 22096075]  [MGI Ref ID J:178999]

Apelqvist A; Li H; Sommer L; Beatus P; Anderson DJ; Honjo T; Hrabe de Angelis M; Lendahl U; Edlund H. 1999. Notch signalling controls pancreatic cell differentiation. Nature 400(6747):877-81. [PubMed: 10476967]  [MGI Ref ID J:57072]

Barrantes IB; Elia AJ; Wunsch K; De Angelis MH; Mak TW; Rossant J; Conlon RA; Gossler A; de la Pompa JL. 1999. Interaction between Notch signalling and Lunatic fringe during somite boundary formation in the mouse. Curr Biol 9(9):470-80. [PubMed: 10330372]  [MGI Ref ID J:54606]

Brohl D; Vasyutina E; Czajkowski MT; Griger J; Rassek C; Rahn HP; Purfurst B; Wende H; Birchmeier C. 2012. Colonization of the satellite cell niche by skeletal muscle progenitor cells depends on Notch signals. Dev Cell 23(3):469-81. [PubMed: 22940113]  [MGI Ref ID J:188916]

Chen J; Kang L; Zhang N. 2005. Negative feedback loop formed by Lunatic fringe and Hes7 controls their oscillatory expression during somitogenesis. Genesis 43(4):196-204. [PubMed: 16342160]  [MGI Ref ID J:104451]

Cheng HT; Kim M; Valerius MT; Surendran K; Schuster-Gossler K; Gossler A; McMahon AP; Kopan R. 2007. Notch2, but not Notch1, is required for proximal fate acquisition in the mammalian nephron. Development 134(4):801-11. [PubMed: 17229764]  [MGI Ref ID J:119907]

Cordes R; Schuster-Gossler K; Serth K; Gossler A. 2004. Specification of vertebral identity is coupled to Notch signalling and the segmentation clock. Development 131(6):1221-33. [PubMed: 14960495]  [MGI Ref ID J:88580]

De Bellard M; Ching W; Gossler A; Bronner-Fraser M. 2002. Disruption of segmental neural crest migration and ephrin expression in delta-1 null mice. Dev Biol 249(1):121. [PubMed: 12217323]  [MGI Ref ID J:78768]

Estrach S; Cordes R; Hozumi K; Gossler A; Watt FM. 2008. Role of the Notch ligand Delta1 in embryonic and adult mouse epidermis. J Invest Dermatol 128(4):825-32. [PubMed: 17960184]  [MGI Ref ID J:135515]

Feyerabend TB; Terszowski G; Tietz A; Blum C; Luche H; Gossler A; Gale NW; Radtke F; Fehling HJ; Rodewald HR. 2009. Deletion of Notch1 converts pro-T cells to dendritic cells and promotes thymic B cells by cell-extrinsic and cell-intrinsic mechanisms. Immunity 30(1):67-79. [PubMed: 19110448]  [MGI Ref ID J:143731]

Huppert SS; Ilagan MX; De Strooper B; Kopan R. 2005. Analysis of Notch Function in Presomitic Mesoderm Suggests a gamma-Secretase-Independent Role for Presenilins in Somite Differentiation. Dev Cell 8(5):677-88. [PubMed: 15866159]  [MGI Ref ID J:98438]

Jouve C; Palmeirim I; Henrique D; Beckers J; Gossler A; Ish-Horowicz D; Pourquie O. 2000. Notch signalling is required for cyclic expression of the hairy-like gene HES1 in the presomitic mesoderm. Development 127(7):1421-9. [PubMed: 10704388]  [MGI Ref ID J:60836]

Kiernan AE; Cordes R; Kopan R; Gossler A; Gridley T. 2005. The Notch ligands DLL1 and JAG2 act synergistically to regulate hair cell development in the mammalian inner ear. Development 132(19):4353-62. [PubMed: 16141228]  [MGI Ref ID J:132241]

Koch U; Fiorini E; Benedito R; Besseyrias V; Schuster-Gossler K; Pierres M; Manley NR; Duarte A; Macdonald HR; Radtke F. 2008. Delta-like 4 is the essential, nonredundant ligand for Notch1 during thymic T cell lineage commitment. J Exp Med 205(11):2515-23. [PubMed: 18824585]  [MGI Ref ID J:143472]

Krebs LT; Iwai N; Nonaka S; Welsh IC; Lan Y; Jiang R; Saijoh Y; O'Brien TP; Hamada H; Gridley T. 2003. Notch signaling regulates left-right asymmetry determination by inducing Nodal expression. Genes Dev 17(10):1207-12. [PubMed: 12730124]  [MGI Ref ID J:83358]

Leimeister C; Dale K; Fischer A; Klamt B; Hrabe de Angelis M; Radtke F; McGrew MJ; Pourquie O; Gessler M. 2000. Oscillating expression of c-hey2 in the presomitic mesoderm suggests that the segmentation clock may use combinatorial signaling through multiple interacting bHLH factors Dev Biol 227(1):91-103. [PubMed: 11076679]  [MGI Ref ID J:65682]

Leimeister C; Schumacher N; Steidl C; Gessler M. 2000. Analysis of HeyL expression in wild-type and notch pathway mutant mouse embryos Mech Dev 98(1-2):175-8. [PubMed: 11044625]  [MGI Ref ID J:65645]

Limbourg A; Ploom M; Elligsen D; Sorensen I; Ziegelhoeffer T; Gossler A; Drexler H; Limbourg FP. 2007. Notch ligand Delta-like 1 is essential for postnatal arteriogenesis. Circ Res 100(3):363-71. [PubMed: 17234965]  [MGI Ref ID J:133690]

Machka C; Kersten M; Zobawa M; Harder A; Horsch M; Halder T; Lottspeich F; Hrabe de Angelis M; Beckers J. 2005. Identification of Dll1 (Delta1) target genes during mouse embryogenesis using differential expression profiling. Gene Expr Patterns 6(1):94-101. [PubMed: 15979417]  [MGI Ref ID J:103128]

Marklund U; Hansson EM; Sundstrom E; de Angelis MH; Przemeck GK; Lendahl U; Muhr J; Ericson J. 2010. Domain-specific control of neurogenesis achieved through patterned regulation of Notch ligand expression. Development 137(3):437-45. [PubMed: 20081190]  [MGI Ref ID J:156172]

McCright B; Gao X; Shen L; Lozier J; Lan Y; Maguire M; Herzlinger D; Weinmaster G; Jiang R; Gridley T. 2001. Defects in development of the kidney, heart and eye vasculature in mice homozygous for a hypomorphic Notch2 mutation. Development 128(4):491-502. [PubMed: 11171333]  [MGI Ref ID J:67157]

Mielcarek M; Piotrowska I; Schneider A; Gunther S; Braun T. 2009. VITO-2, a new SID domain protein, is expressed in the myogenic lineage during early mouse embryonic development. Gene Expr Patterns 9(3):129-37. [PubMed: 19118645]  [MGI Ref ID J:144198]

Morrison A; Hodgetts C; Gossler A; Hrabe de Angelis M; Lewis J. 1999. Expression of Delta1 and Serrate1 (Jagged1) in the mouse inner ear. Mech Dev 84(1-2):169-72. [PubMed: 10473135]  [MGI Ref ID J:56415]

Mouse Genome Informatics and the Europhenome Mouse Phenotyping Resource. 2010. Obtaining and Loading Phenotype Annotations from Europhenome Database Release :.  [MGI Ref ID J:165965]

Napp LC; Augustynik M; Paesler F; Krishnasamy K; Woiterski J; Limbourg A; Bauersachs J; Drexler H; Le Noble F; Limbourg FP. 2012. Extrinsic Notch ligand Delta-like 1 regulates tip cell selection and vascular branching morphogenesis. Circ Res 110(4):530-5. [PubMed: 22282195]  [MGI Ref ID J:192694]

Okubo Y; Sugawara T; Abe-Koduka N; Kanno J; Kimura A; Saga Y. 2012. Lfng regulates the synchronized oscillation of the mouse segmentation clock via trans-repression of Notch signalling. Nat Commun 3:1141. [PubMed: 23072809]  [MGI Ref ID J:205623]

Pfister S; Przemeck GK; Gerber JK; Beckers J; Adamski J; Hrabe de Angelis M. 2003. Interaction of the MAGUK family member Acvrinp1 and the cytoplasmic domain of the Notch ligand Delta1. J Mol Biol 333(2):229-35. [PubMed: 14529612]  [MGI Ref ID J:114126]

Przemeck GK; Heinzmann U; Beckers J; Hrabe De Angelis M. 2003. Node and midline defects are associated with left-right development in Delta1 mutant embryos. Development 130(1):3-13. [PubMed: 12441287]  [MGI Ref ID J:80018]

Raya A; Kawakami Y; Rodriguez-Esteban C; Buscher D; Koth CM; Itoh T; Morita M; Raya RM; Dubova I; Bessa JG; de la Pompa JL; Belmonte JC. 2003. Notch activity induces Nodal expression and mediates the establishment of left-right asymmetry in vertebrate embryos. Genes Dev 17(10):1213-8. [PubMed: 12730123]  [MGI Ref ID J:83387]

Rocha SF; Lopes SS; Gossler A; Henrique D. 2009. Dll1 and Dll4 function sequentially in the retina and pV2 domain of the spinal cord to regulate neurogenesis and create cell diversity. Dev Biol 328(1):54-65. [PubMed: 19389377]  [MGI Ref ID J:149456]

Rubio-Aliaga I; Przemeck GK; Fuchs H; Gailus-Durner V; Adler T; Hans W; Horsch M; Rathkolb B; Rozman J; Schrewe A; Wagner S; Hoelter SM; Becker L; Klopstock T; Wurst W; Wolf E; Klingenspor M; Ivandic BT; Busch DH; Beckers J; Hrabe de Angelis M. 2009. Dll1 haploinsufficiency in adult mice leads to a complex phenotype affecting metabolic and immunological processes. PLoS One 4(6):e6054. [PubMed: 19562077]  [MGI Ref ID J:150183]

Rubio-Aliaga I; Soewarto D; Wagner S; Klaften M; Fuchs H; Kalaydjiev S; Busch DH; Klempt M; Rathkolb B; Wolf E; Abe K; Zeiser S; Przemeck GK; Beckers J; de Angelis MH. 2007. A genetic screen for modifiers of the delta1-dependent notch signaling function in the mouse. Genetics 175(3):1451-63. [PubMed: 17179084]  [MGI Ref ID J:119997]

Schuster-Gossler K; Cordes R; Gossler A. 2007. Premature myogenic differentiation and depletion of progenitor cells cause severe muscle hypotrophy in Delta1 mutants. Proc Natl Acad Sci U S A 104(2):537-42. [PubMed: 17194759]  [MGI Ref ID J:119082]

Schwarting GA; Gridley T; Henion TR. 2007. Notch1 expression and ligand interactions in progenitor cells of the mouse olfactory epithelium. J Mol Histol 38(6):543-53. [PubMed: 17605079]  [MGI Ref ID J:130594]

Sorensen I; Adams RH; Gossler A. 2009. DLL1-mediated Notch activation regulates endothelial identity in mouse fetal arteries. Blood 113(22):5680-8. [PubMed: 19144989]  [MGI Ref ID J:148902]

Stamataki D; Holder M; Hodgetts C; Jeffery R; Nye E; Spencer-Dene B; Winton DJ; Lewis J. 2011. Delta1 expression, cell cycle exit, and commitment to a specific secretory fate coincide within a few hours in the mouse intestinal stem cell system. PLoS One 6(9):e24484. [PubMed: 21915337]  [MGI Ref ID J:177887]

Takahashi Y; Yasuhiko Y; Kitajima S; Kanno J; Saga Y. 2007. Appropriate suppression of Notch signaling by Mesp factors is essential for stripe pattern formation leading to segment boundary formation. Dev Biol 304(2):593-603. [PubMed: 17306789]  [MGI Ref ID J:122532]

Tan JB ; Xu K ; Cretegny K ; Visan I ; Yuan JS ; Egan SE ; Guidos CJ. 2009. Lunatic and manic fringe cooperatively enhance marginal zone B cell precursor competition for delta-like 1 in splenic endothelial niches. Immunity 30(2):254-63. [PubMed: 19217325]  [MGI Ref ID J:146621]

Xu K; Usary J; Kousis PC; Prat A; Wang DY; Adams JR; Wang W; Loch AJ; Deng T; Zhao W; Cardiff RD; Yoon K; Gaiano N; Ling V; Beyene J; Zacksenhaus E; Gridley T; Leong WL; Guidos CJ; Perou CM; Egan SE. 2012. Lunatic fringe deficiency cooperates with the Met/Caveolin gene amplicon to induce basal-like breast cancer. Cancer Cell 21(5):626-41. [PubMed: 22624713]  [MGI Ref ID J:189299]

Yun K; Fischman S; Johnson J; De Angelis MH; Weinmaster G; Rubenstein JL. 2002. Modulation of the notch signaling by Mash1 and Dlx1/2 regulates sequential specification and differentiation of progenitor cell types in the subcortical telencephalon. Development 129(21):5029-40. [PubMed: 12397111]  [MGI Ref ID J:79854]

Zhang N; Norton CR; Gridley T. 2002. Segmentation defects of Notch pathway mutants and absence of a synergistic phenotype in lunatic fringe/radical fringe double mutant mice. Genesis 33(1):21-8. [PubMed: 12001066]  [MGI Ref ID J:77247]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

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

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.

Embryos

Price (US dollars $)
Frozen Embryo $1600.00

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
  • 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.

Embryos

Price (US dollars $)
Frozen Embryo $2080.00

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
  • 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
   000664 C57BL/6J
 
  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


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.


(6.5)