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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Vhltm1Wml
targeted mutation 1, W Marston Linehan
MGI:1857702
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Vhltm1Wml/Vhltm1Wml involves: 129S1/Sv * C57BL/6 MGI:2176441
ht2
Vhltm1Wml/Vhl+ B6;129 MGI:3038945


Genotype
MGI:2176441
hm1
Allelic
Composition
Vhltm1Wml/Vhltm1Wml
Genetic
Background
involves: 129S1/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Vhltm1Wml mutation (0 available); any Vhl mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Placental histopathology of normal and Vhltm1Wml/Vhltm1Wml embryos

mortality/aging
• death between E10.5 and E12.5, likely due to abnormal placental development (J:42486)
• death between E10.5 and E12.5, likely due to abnormal placental development (J:42486)

embryogenesis
• failed embryonic vasculogenesis, with hemorrhage evident by E11.5 to E12.5 (J:42486)
• lacked embryonic endothelium and blood vessels (J:42486)
• lacked embryonic endothelium and blood vessels (J:42486)
• failed embryonic vasculogenesis, with hemorrhage evident by E11.5 to E12.5 (J:42486)
• evident between E9.5 and E10.5 (J:42486)
• evident between E9.5 and E10.5 (J:42486)
• appeared normal until E9.5, but did not progress developmentally (J:42486)
• appeared normal until E9.5, but did not progress developmentally (J:42486)

cardiovascular system
• failed embryonic vasculogenesis, with hemorrhage evident by E11.5 to E12.5 (J:42486)
• lacked embryonic endothelium and blood vessels (J:42486)
• failed embryonic vasculogenesis, with hemorrhage evident by E11.5 to E12.5 (J:42486)
• lacked embryonic endothelium and blood vessels (J:42486)
• hemorrhagic placenta (J:42486)
• hemorrhagic placenta (J:42486)




Genotype
MGI:3038945
ht2
Allelic
Composition
Vhltm1Wml/Vhl+
Genetic
Background
B6;129
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Vhltm1Wml mutation (0 available); any Vhl mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• increased incidence of vascular neoplasms in the liver, uterus, ovary, spleen and heart in response to streptozotocin, compared to controls (J:88492)
• highest incidence and number found in liver (J:88492)
• lesions seen: angiectasia, hemangisarcoma, hemangioma (J:88492)
• no increase in renal lesions in response to streptozotocin, compared to controls (J:88492)
• increased incidence of vascular neoplasms in the liver, uterus, ovary, spleen and heart in response to streptozotocin, compared to controls (J:88492)
• highest incidence and number found in liver (J:88492)
• lesions seen: angiectasia, hemangisarcoma, hemangioma (J:88492)
• no increase in renal lesions in response to streptozotocin, compared to controls (J:88492)

homeostasis/metabolism
• increased incidence of vascular neoplasms in the liver, uterus, ovary, spleen and heart in response to streptozotocin, compared to controls (J:88492)
• highest incidence and number found in liver (J:88492)
• lesions seen: angiectasia, hemangisarcoma, hemangioma (J:88492)
• no increase in renal lesions in response to streptozotocin, compared to controls (J:88492)
• increased incidence of vascular neoplasms in the liver, uterus, ovary, spleen and heart in response to streptozotocin, compared to controls (J:88492)
• highest incidence and number found in liver (J:88492)
• lesions seen: angiectasia, hemangisarcoma, hemangioma (J:88492)
• no increase in renal lesions in response to streptozotocin, compared to controls (J:88492)

Mouse Models of Human Disease
OMIM ID Ref(s)
Von Hippel-Lindau Syndrome; VHL 193300 J:42486 , J:88492





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last database update
01/26/2016
MGI 6.02
The Jackson Laboratory