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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Cdh5tm3(Cdh5/Ctnna1)Dvst
targeted mutation 3, Dietmar Vestweber
MGI:5294790
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Cdh5tm3(Cdh5/Ctnna1)Dvst/Cdh5tm3(Cdh5/Ctnna1)Dvst B6.Cg-Cdh5tm3(Cdh5/Ctnna1)Dvst MGI:5294810
hm2
Cdh5tm3(Cdh5/Ctnna1)Dvst/Cdh5tm3(Cdh5/Ctnna1)Dvst involves: 129 * C57BL/6 MGI:5294809


Genotype
MGI:5294810
hm1
Allelic
Composition
Cdh5tm3(Cdh5/Ctnna1)Dvst/Cdh5tm3(Cdh5/Ctnna1)Dvst
Genetic
Background
B6.Cg-Cdh5tm3(Cdh5/Ctnna1)Dvst
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdh5tm3(Cdh5/Ctnna1)Dvst mutation (0 available); any Cdh5 mutation (59 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• at E10.5, homozygotes display no gross abnormalities in angiogenesis, as shown by PECAM-1 whole-mount immunostaining
• at E13.5 and E14.5, analysis of the area covered by endomucin-positive vessels in fetal skin revealed no defects in angiogenesis
• no heart defects in cushion formation are detected at E11.0

mortality/aging
• homozygotes die late during fetal development
• only 13 of 18 homozygotes are viable at E16.5, with no homozygotes identified at P21
• homozygotes start dying around E13.5
• however, homozygotes are viable and phenotypically normal at E9.5
• Background Sensitivity: 100% unlike on a mixed background

hematopoietic system
• at E13.5, homozygotes display a reduced ratio of hematopoietic to hepatoblastic cells in fetal liver, indicating impaired fetal liver hematopoiesis
• however, at E10.5, endothelial to hematopoietic transition in the dorsal aorta is normal
• at E13.5, the frequency of clonogenic progenitor cells (CFUs) is significantly increased in fetal blood and reduced in fetal liver
• however, the relative abundance of different progenitor types is not changed in fetal liver
• at E13.5, homozygotes display a significant increase of c-Kit-positive, lineage marker-negative (c-Kit+ lin-) hematopoietic progenitors in fetal circulation
• at E13.5, hematopoietic stem and progenitor cells (HSPCs) accumulate in the fetal circulation suggesting that their entry into the fetal liver is blocked
• however, no defects in the generation of HSPCs from hemogenic endothelium or their differentiation into multiple hematopoietic lineages are observed

homeostasis/metabolism
• starting at E13.5, homozygotes display edema formation of variable severity as a result of disturbed lymphatic vessel development
• 64% of mutant fetuses at E13.5 and ~80% at E14.5 exhibit visible edema

immune system
• starting at E13.5, homozygotes display progressive disruption of lymphatic vessel integrity in fetal skin
• although the first or initial Prox1+ LECs are able to leave the cardinal vein and migrate to the site of the first lymphatic vessel formation, morphogenesis of the first large lymphatic vessels, pTD (primordial thoracic duct) and PLLV (peripheral longitudinal lymphatic vessel), is impaired
• at E12.0, lumenization pTD and PLLV is severely impaired
• pTD shows a discontinuous lumen with multiple constrictions and appears fragmented while abnormal structures of lymphatic vessels are formed from the PLLV
• at E13.5, lymphatic endothelial cells (LECs) are present but do not form a branched network as in controls
• at E14.5, only islands of disconnected LECs are detectable, unlike in control fetuses where further maturation of the lymphatic vascular plexus is observed
• however, at 13.5 and E14.5, the blood vasculature and VE-cadherin staining of lymphatic junctions is normal

liver/biliary system
• at E14.5, all homozygotes show a variable reduction in fetal liver size
• in 50% of homozygotes, average fetal liver weight/cellularity is down to 20%-50% of wild-type controls
• at E13.5 and E14.5, average fetal liver weight is significantly reduced
• at E13.5 and E14.5, average fetal liver cellularity is significantly reduced




Genotype
MGI:5294809
hm2
Allelic
Composition
Cdh5tm3(Cdh5/Ctnna1)Dvst/Cdh5tm3(Cdh5/Ctnna1)Dvst
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdh5tm3(Cdh5/Ctnna1)Dvst mutation (0 available); any Cdh5 mutation (59 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• fewer than expected mice are produced from mating homozygotes or heterozygotes
• Background Sensitivity: some mice are viable unlike on a congenic C57BL/6 background
• however, viable mice are healthy and fertile

immune system
N
• whole-mount preparations of ear skin from adult mice revealed no differences for the characteristic VE-cadherin and PECAM-1 staining of button-like junctions in initial lymphatics relative to wild-type controls
• LPS- or dinitrofluorbenzene-treated mice exhibit reduced recruitment of neutrophils or lymphocytes into inflamed lung or skin compared with similarly treated wild-type mice
• paracellular diapedesis is blocked
• however, leukocytes exhibit normal naive homing, adhesion, rolling, and transcellular diapedesis
• leukocyte extravasation is reduced in IL1b-inflamed cremaster, lungs of LPS-treated mice, or skin of dinitrofluorbenzene-treated mice compared to in similarly treated wild-type mice
• in culture, lymphatic endothelial cells (LECs) isolated from lungs of 7- to 9-week-old mice and stained for VE-cadherin and lymphatic markers show no difference in the recruitment of VEC-alpha-C and VE-cadherin to junctions; however, mutant LECs appear more widespread than control LECs
• video imaging over a 24-hr period confirmed a more intense spreading of mutant LECs
• however, no differences in LEC motility are observed

cardiovascular system
• skin fails to exhibit vascular permeability induced by VEGF and histamine unlike in control skin

integument
• skin fails to exhibit vascular permeability induced by VEGF and histamine unlike in control skin

hematopoietic system
• LPS- or dinitrofluorbenzene-treated mice exhibit reduced recruitment of neutrophils or lymphocytes into inflamed lung or skin compared with similarly treated wild-type mice
• paracellular diapedesis is blocked
• however, leukocytes exhibit normal naive homing, adhesion, rolling, and transcellular diapedesis
• leukocyte extravasation is reduced in IL1b-inflamed cremaster, lungs of LPS-treated mice, or skin of dinitrofluorbenzene-treated mice compared to in similarly treated wild-type mice

cellular
• LPS- or dinitrofluorbenzene-treated mice exhibit reduced recruitment of neutrophils or lymphocytes into inflamed lung or skin compared with similarly treated wild-type mice
• paracellular diapedesis is blocked
• however, leukocytes exhibit normal naive homing, adhesion, rolling, and transcellular diapedesis
• leukocyte extravasation is reduced in IL1b-inflamed cremaster, lungs of LPS-treated mice, or skin of dinitrofluorbenzene-treated mice compared to in similarly treated wild-type mice





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last database update
10/29/2024
MGI 6.24
The Jackson Laboratory