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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Rae1tm1Jvd
targeted mutation 1, Jan M A van Deursen
MGI:3619246
Summary 5 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Rae1tm1Jvd/Rae1tm1Jvd Not Specified MGI:3620036
ht2
Rae1tm1Jvd/Rae1+ Not Specified MGI:3620037
cx3
Nup88em1Jvd/Nup88+
Nup98tm1Jvd/Nup98+
Rae1tm1Jvd/Rae1+
involves: C57BL/6 MGI:6377639
cx4
Bub3tm1Jvd/Bub3+
Rae1tm1Jvd/Rae1+
Not Specified MGI:3620038
cx5
Nup98tm1Jvd/Nup98+
Rae1tm1Jvd/Rae1+
Not Specified MGI:6377636


Genotype
MGI:3620036
hm1
Allelic
Composition
Rae1tm1Jvd/Rae1tm1Jvd
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rae1tm1Jvd mutation (0 available); any Rae1 mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• homozygous embryos are present at E3.5 but absent by E8.5

embryo
• in culture the inner cell mass fails to expand from E6.5 to E8.5 and instead degenerates
• however, the trophoblast cells develop normally




Genotype
MGI:3620037
ht2
Allelic
Composition
Rae1tm1Jvd/Rae1+
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rae1tm1Jvd mutation (0 available); any Rae1 mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• in heterozygous MEFs after 5 passages about 20% of metaphases are aneuploid compared to about 9% in wild-type cells and a wider range of nonmodal chromosome numbers is seen (J:81546)
• at 5 months of age, 9% of splenocytes are aneuploid (J:81546)
• the number of aneuploid splenocytes increases from 9% at 5 months to 33% at 24 months compared to only 3% in wild-type mice at 35 months (J:105717)
• after 12 hours of treatment with 200 ng/ml nocodazole (induces spindle damage) only 2.5% of heterozygous MEFs are arrested compared to 15% of wild-type cells and after 4 hours in serum without nocodazole (recovery phase) more cells are present with 4N DNA content suggesting progression to G1 without cell division (J:81546)
• overexpression of Rae1 can rescue the mitotic checkpoint defect (J:81546)
• after nocodazole treatment the time for 50% of cells to exit prometaphase arrest is reduced to 3 hours compared to 7.2 hours for wild-type MEFs (J:105717)
• lagging chromosomes are seen in 5% of anaphase figures compared to 2% of wild-type figures (J:81546)
• in splenocytes prematurely separated sister chromatids increase from 0 at 5 months to being present in 10-11% of metaphases at 24-27 months compared to 0 at 27 months and only 4% at 35 months in wild-type (J:105717)
• however, no chromosome breaks or fusions are seen at 24 months of age (J:105717)

neoplasm
• a single application of 50 ul of 0.5% DMBA at P5 results in an increased incidence of lung tumors and more tumors per animal in heterozygotes compared to wild-type mice
• however, no difference in spontaneous tumor incidence is seen compared to wild-type mice

homeostasis/metabolism
• a single application of 50 ul of 0.5% DMBA at P5 results in an increased incidence of lung tumors and more tumors per animal in heterozygotes compared to wild-type mice
• however, no difference in spontaneous tumor incidence is seen compared to wild-type mice




Genotype
MGI:6377639
cx3
Allelic
Composition
Nup88em1Jvd/Nup88+
Nup98tm1Jvd/Nup98+
Rae1tm1Jvd/Rae1+
Genetic
Background
involves: C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nup88em1Jvd mutation (0 available); any Nup88 mutation (44 available)
Nup98tm1Jvd mutation (0 available); any Nup98 mutation (146 available)
Rae1tm1Jvd mutation (0 available); any Rae1 mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• chromosome segregation errors are reduced to 18% from 37% in double Rae1tm1Jvd Nup98tm1Jvd heterozygotes and the mitotic checkpoint is fully restored




Genotype
MGI:3620038
cx4
Allelic
Composition
Bub3tm1Jvd/Bub3+
Rae1tm1Jvd/Rae1+
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bub3tm1Jvd mutation (0 available); any Bub3 mutation (23 available)
Rae1tm1Jvd mutation (0 available); any Rae1 mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Reduced lifespan, cataract, lordokyphosis and cachexia in Bub3tm1Jvd/Bub3+ Rae1tm1Jvd/Rae1+ mice

mortality/aging
• seen in the second year of life

cellular
• in double heterozygous MEFs after 5 passages aneuploid cells are increased by 32% compared to wild-type cells and a wider range of nonmodal chromosome numbers is seen compared to single heterozygous or wild-type MEFs (J:81546)
• at 5 months of age, 37% of splenocytes are aneuploid compared to 9% in single heterozygotes (J:81546)
• the number of aneuploid splenocytes increases from 37% at 5 months to 47% at 24 months compared to only 3% in wild-type mice at 35 months (J:105717)
• after nocodazole treatment the time for 50% of cells to exit prometaphase arrest is reduced to 2.2 hours compared to 7.2 hours for wild-type MEFs
• prematurely separated sister chromatids are seen in 19% and 13% of mitotic figures from MEFs and splenocytes (at 5 months of age), respectively (J:81546)
• lagging chromosomes are seen in 15% of anaphase figures compared to 5% of single heterozygous and 2% of wild-type figures (J:81546)
• in splenocytes prematurely separated sister chromatids increase from 14% at 5 months to being present in 24% of metaphases at 24 months compared to 0 at 27 months and only 4% at 35 months in wild-type (J:105717)
• however, no chromosome breaks or fusions are seen at 24 months of age (J:105717)
• 47% of anaphases have multiple lagging chromosomes compared to 0% in wild-type MEFs (J:105717)
• double heterozygous MEFs grow slower than single heterozygous or wild-type MEFs
• at passage 5 and 7 increased expression of senescence related genes in MEFs is seen
• at passage 7 but not passage 3, double heterozygous MEFs grow slower than single heterozygous or wild-type MEFs

adipose tissue
• decreased thickness of the subcutaneous adipose tissue
• at 27 months of age a dramatic decrease in body fat is seen

growth/size/body
• body weight is similar to wild-type at 5 months of age but significantly lower by 24 months of age

muscle
• clear signs of skeletal muscle degeneration and atrophy are seen in mice with lordokyphosis
• clear signs of skeletal muscle degeneration and atrophy are seen in mice with lordokyphosis

skeleton
• lordokyphosis is seen at an earlier age and with increased severity compared to single heterozygous or wild-type mice

vision/eye
• incidence of cataract formation is increased and the latency is decreased compared to single heterozygotes

neoplasm
• a single application of 50 ul of 0.5% DMBA at P5 results in an increased incidence of lung tumors and more tumors per animal in double heterozygotes compared to wild-type mice
• however, no difference in spontaneous tumor incidence is seen compared to wild-type mice

homeostasis/metabolism
• a single application of 50 ul of 0.5% DMBA at P5 results in an increased incidence of lung tumors and more tumors per animal in double heterozygotes compared to wild-type mice
• however, no difference in spontaneous tumor incidence is seen compared to wild-type mice

integument
• decreased thickness of the subcutaneous adipose tissue
• from 5 to 27 months of age dermal thickness decreases by 21% lower compared a decrease of 9% in wild-type mice




Genotype
MGI:6377636
cx5
Allelic
Composition
Nup98tm1Jvd/Nup98+
Rae1tm1Jvd/Rae1+
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nup98tm1Jvd mutation (0 available); any Nup98 mutation (146 available)
Rae1tm1Jvd mutation (0 available); any Rae1 mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• MEFs exhibit mitotic checkpoint defects
• MEFs have increased rates of chromatin bridges and lagging chromosomes indicating chromosome segregation errors
• incomplete centrosome separation is increased in MEFs
• MEFs treated with the PLK1 inhibitor BI2536 show restoration of normal centrosome separation
• MEFs exhibit more frequent spindle geometry defects showing mitotic spindle asymmetry





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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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last database update
11/19/2024
MGI 6.24
The Jackson Laboratory