Strain Detail Sheet

Phenotype:
Homozygous phenotype: Mice die at midgestation due to vascularization failure marked by growth retardation and disorganized vascular structures.

Heterozygous phenotype: The life expectancy, fertility, and gross appearance of the viable heterozygous progeny appeared normal.

Mammalian Phenotype Terms:(provided by MGI)      Extend all MPTs
      assigned by genotype

The following phenotype information may relate to one or more alleles on a genetic background differing from this MMRRC strain.

Ptprj^tm1Taka/Ptprj⁺

        involves: 129S6/SvEvTac * C57BL/6

• mortality/aging
  • partial embryonic lethality during organogenesis (MGI Ref ID J:82356)
    • a fraction of heterozygotes die in utero, as suggested by a shift in the ratio of viable wild-type to heterozygous embryos after E11.5 (44.9% versus 55.1%) coupled with resorption embryo remnants
    • however, no vascular abnormalities are detected in heterozygous embryos between E8.25 and E10.5
    • in addition, surviving heterozygotes are fertile, grossly normal, and exhibit a normal lifespan

Ptprj^tm1Taka/Ptprj^tm1Taka

        involves: 129S6/SvEvTac

• mortality/aging
  • complete embryonic lethality during organogenesis (MGI Ref ID J:82356)
    • homozygous mutant embryos are recovered at the expected Mendelian frequencies at E8.5, E9.5, and E10.5, but are completely lost by E11.5
• growth/size phenotype
  • decreased embryo size (MGI Ref ID J:82356)
    • as early as E9.5, mutant embryos are significantly smaller than wild-type embryos
  • embryonic growth retardation (MGI Ref ID J:82356)
    • by E10.5, homozygotes display severe growth retardation relative to wild-type controls
• cardiovascular system phenotype
  • abnormal endocardium morphology (MGI Ref ID J:82356)
    • at E9.0, homozygotes display abnormal endocardial projections extending beyond the cardiac jelly
    • at E9.5, a less intricately folded endocardium, and scattered, disconnected endocardial cells are observed
    • mutant endocardial cells exhibit a rounded and shortened morphology relative to wild-type endocardial cells
  • abnormal heart development (MGI Ref ID J:82356)
    • absent atrioventricular cushions (MGI Ref ID J:82356)
      • at E9.5, mutant developing hearts lacked mesenchymal cushion formation adjacent to the atrioventricular canal
    • delayed heart looping (MGI Ref ID J:82356)
      • at E8.25, homozygotes exhibit delayed cardiac looping relative to wild-type controls
  • abnormal myocardial trabeculae morphology (MGI Ref ID J:82356)
    • at E9.5, homozygotes exhibit disorganized myocardial trabeculation, lacking finger-like trabeculae lined by endocardial cells
  • abnormal pericyte morphology (MGI Ref ID J:82356)
    • at E9.0, mutant yolk sacs show a slight decrease in the number of pericytes (PCs) relative to wild-type yolk sacs
    • at E9.0, mutant yolk sacs exhibit round and sparsely distributed PCs between the endoderm and endothelium
    • by E9.5, mutant PCs are poorly elongated, fail to encircle the endothelial vessels, and are loosely associated with the endothelium in yolk sacs
  • abnormal vascular development (MGI Ref ID J:82356)
    • at E8.25-E9.0, homozygotes display vascular development defects, including a poorly formed cerebral vascular plexus
    • at E9.0, a narrow dorsal aorta, enlarged intersomitic networks, and dorsally fused intersomitic vessels are observed
    • at E9.5, homogeneously enlarged primitive vessels defective in vascular remodeling and branching, and impaired pericyte investment adjacent to endothelial structures are observed
    • abnormal dorsal aorta morphology (MGI Ref ID J:82356)
      • at E9.0, homozygotes display a collapsed dorsal aorta which includes abundant endothelial cells and disorganized intersomitic sprouts
      • at E9.5-E10.5, the dorsal aorta is atrophic and resembles a disorganized string of aligned endothelial cells with fewer intersomitic sprouts; by E10.5, its outline is discontinuous
    • abnormal vascular branc hing morphogenesis (MGI Ref ID J:82356)
      • at E9.5, homozygotes show absence of large branching vessels, and accumulation of primitive blood cells in the yolk sac
      • failure of vascular branching (MGI Ref ID J:82356)
        • at E9.5-E10.5, mutant cerebral vessels lack branching vessels of large diameters
        • by E10.5, mutant peripheral vessels are oversized, disorganized, and densely interconnected
    • abnormal vitelline vasculature morphology (MGI Ref ID J:82356)
      • at E9.5, homozygotes display accumulation of primitive blood cells in the yolk sac
      • as early as E8.25, homozygotes display focally enlarged and fused yolk sac vessels
      • abnormal vitelline vascular remodeling (MGI Ref ID J:82356)
        • at E9.0, mutant yolk sac vascular networks exhibit homogeneously sized and focally enlarged endothelial vessels, instead of a differentiated vasculature composed of large- and small-diameter vessels of interconnecting cells
        • at E9.5-E10.5, mutant yolk sac vessels fail to mature and to form large vitelline vessels and a capillary network; instead, endothelial structures are abnormally expanded and fused and a few avascular areas are observed between vessels
        • at E9.0, vitelline vessels are reduced in number but display an increase in the % of total vessels of larger diameters (>800 µm²)
  • abnormal vascular endothelial cell morphology (MGI Ref ID J:82356)
    • at E9.5, mutant yolk sacs display a discontinuity in endothelial cells
    • by E10.5, endothelial cells are detached from subjacent mesoepithelium
    • increased vascular endothelial cell number (MGI Ref ID J:82356)
      • at E9.0, mutant yolk sac vessels exhibit a 58% increase in the number of endothelial cells per millimeter of vessel length, as determined by Ki67 staining
      • however, no difference in endodermal cell numbers is observed
  • abnormal vascular smooth muscle morphology (MGI Ref ID J:82356)
    • at E9.0, mutant yolk sacs exhibit round and sparsely distributed vSMCs between the endoderm and endothelium
    • by E9.5, mutant vSMCs are poorly elongated, fail to encircle the endothelial vessels, and are loosely associated with the endothelium in mutant yolk sacs
    • vascular smooth muscle cell hypoplasia (MGI Ref ID J:82356)
      • at E9.0, mutant yolk sacs show a slight decrease in the number of vSMCs relative to wild-type yolk sacs
      • only a few vSMCs are detected around the mutant dorsal aorta
  • distended pericardium (MGI Ref ID J:82356)
    • at E9.5, homozygotes display a distended pericardium
    • by E10.5, a prominent extension of the pericardial sac is observed
  • enlarged pericardium (MGI Ref ID J:82356)
    • at E9.5, homozygotes display an enlarged pericardial cavity
  • thin myocardium (MGI Ref ID J:82356)
    • at E9.5, the thickness of the myocardial wall is reduced while the space between the endocardium and myocardium is increased
• embryogenesis phenotype
  • abnormal vitelline vasculature morphology (MGI Ref ID J:82356)
    • at E9.5, homozygotes display accumulation of primitive blood cells in the yolk sac
    • as early as E8.25, homozygotes display focally enlarged and fused yolk sac vessels
    • abnormal vitelline vascular remodeling (MGI Ref ID J:82356)
      • at E9.0, mutant yolk sac vascular networks exhibit homogeneously sized and focally enlarged endothelial vessels, instead of a differentiated vasculature composed of large- and small-diameter vessels of interconnecting cells
      • at E9.5-E10.5, mutant yolk sac vessels fail to mature and to form large vitelline vessels and a capillary network; instead, endothelial structures are abnormally expanded and fused and a few avascular areas are observed between vessels
      • at E9.0, vitelline vessels are reduced in number but display an increase in the % of total vessels of larger diameters (>800 µm²)
  • decreased embryo size (MGI Ref ID J:82356)
    • as early as E9.5, mutant embryos are significantly smaller than wild-type embryos
  • embryonic growth reta rdation (MGI Ref ID J:82356)
    • by E10.5, homozygotes display severe growth retardation relative to wild-type controls
• muscle phenotype
  • abnormal myocardial trabeculae morphology (MGI Ref ID J:82356)
    • at E9.5, homozygotes exhibit disorganized myocardial trabeculation, lacking finger-like trabeculae lined by endocardial cells
  • abnormal vascular smooth muscle morphology (MGI Ref ID J:82356)
    • at E9.0, mutant yolk sacs exhibit round and sparsely distributed vSMCs between the endoderm and endothelium
    • by E9.5, mutant vSMCs are poorly elongated, fail to encircle the endothelial vessels, and are loosely associated with the endothelium in mutant yolk sacs
    • vascular smooth muscle cell hypoplasia (MGI Ref ID J:82356)
      • at E9.0, mutant yolk sacs show a slight decrease in the number of vSMCs relative to wild-type yolk sacs
      • only a few vSMCs are detected around the mutant dorsal aorta
• craniofacial phenotype
  • microcephaly (MGI Ref ID J:82356)
    • at E9.5, homozygotes exhibit a reduced head size

Founder genetic background: 129X1/SvJ

Strain genetic background: C57BL/6J

Strain Development:
Heterozygous male were backcrossed to C57BL/6J female wildtype for 10 generation.

Donor: Takamune Takahashi, M.D., Vanderbilt University Medical Center

Primary Reference:

Takahashi T; Takahashi K; St John PL; Fleming PA; Tomemori T; Watanabe T; Abrahamson DR; Drake CJ; Shirasawa T; Daniel TO, A mutant receptor tyrosine phosphatase, CD148, causes defects in vascular development., Mol Cell Biol 2003 Mar;23(5):1817-31 (Medline PMID: 12588999)

Additional charges may apply for any special requests. Shipping costs are in addition to the basic distribution/resuscitation fees. Information on shipping costs and any additional charges will be provided by the supplying MMRRC facility.

Click button to Request this one strain. (Use the MMRRC Catalog Search to request more than one strain.) Request this Strain
MMRRC Item # Description	Distribution Fee/unit (US $)	Units	Notes
029875-MU-RESUS Litter recovered from cryo-archive	$2,022.00 Non-Profit $4,109.00 For-Profit	Litter	Recovered litter1; additional fees for any special requests.
029875-MU-SPERM Cryo-preserved spermatozoa	$437.00 Non-Profit $817.00 For-Profit	Aliquot	Approximate quantity.2

¹ The distribution fee covers the expense of resuscitating mice from the cryo-archive; you will receive the resulting litter. The litter will contain at minimum one breedable mutant carrier; the actual number of animals and the gender and genotype ratios will vary. (Typically, multiple breeder pairs can be established from the recovered litter.) Prior to shipment, the MMRRC will provide information about the animals recovered. If you anticipate or find that you need to request specific genotypes, genders or quantities of mice in excess of what is likely from a resuscitated litter, you may discuss available options and pricing with the supplying MMRRC facility.

² An aliquot contains sufficient material (volume and concentration) for at least two IVF or several artificial inseminations (based on our procedures). The MMRRC makes no guarantee concerning success of these procedures when performed outside the MMRRC facilities.

³ An aliquot contains a sufficient number of embryos (in one or more vials and based on the transfer success rate of the MMRRC facility) to transfer to at least two recipients. The MMRRC makes no guarantee concerning embryo transfer success experienced in the recipient investigator's laboratory. Neither gender nor genotype ratios are guaranteed.