Ku80;Prkdc

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Genetic mutants with Ku80, Prkdc alterations

Names of genes are ordered alphabetically. For the order of interventions, please see the specific paper.

Temperature °C
20
Diet
ad libitum
Lifespan (days)
243.6
Phenotype
The dna-pk mice live significantly longer compared to ku80-/- mice in both male (p = 0.01) and females (p = 8.7*10-6) mice.Survival of double knock out mice is identical to ku80-/-
Lifespan comparisons
Double mutant dna-pk(CS);ku80(KO) has a lifespan of 243.6 days, while single mutant dna-pk(CS) has a lifespan of 296.8 days and single mutant ku80(KO) has a lifespan of 238.0 days.
Citation
View abstract
Reiling E et al., 2014, The progeroid phenotype of Ku80 deficiency is dominant over DNA-PKCS deficiency. PLoS One. 9(4):e93568 24740260 Click here to select all mutants from this PubMed ID in the graph
Abstract
Ku80 and DNA-PKCS are both involved in the repair of double strand DNA breaks via the nonhomologous end joining (NHEJ) pathway. While ku80-/- mice exhibit a severely reduced lifespan and size, this phenotype is less pronounced in dna-pkcs-/- mice. However, these observations are based on independent studies with varying genetic backgrounds. Here, we generated ku80-/-, dna-pkcs-/- and double knock out mice in a C57Bl6/J*FVB F1 hybrid background and compared their lifespan, end of life pathology and mutation frequency in liver and spleen using a lacZ reporter. Our data confirm that inactivation of Ku80 and DNA-PKCS causes reduced lifespan and bodyweights, which is most severe in ku80-/- mice. All mutant mice exhibited a strong increase in lymphoma incidence as well as other aging-related pathology (skin epidermal and adnexal atrophy, trabacular bone reduction, kidney tubular anisokaryosis, and cortical and medullar atrophy) and severe lymphoid depletion. LacZ mutation frequency analysis did not show strong differences in mutation frequencies between knock out and wild type mice. The ku80-/- mice had the most severe phenotype and the Ku80-mutation was dominant over the DNA-PKCS-mutation. Presumably, the more severe degenerative effect of Ku80 inactivation on lifespan compared to DNA-PKCS inactivation is caused by additional functions of Ku80 or activity of free Ku70 since both Ku80 and DNA-PKCS are essential for NHEJ.

Temperature °C
20
Diet
ad libitum
Lifespan (days)
230.3
Phenotype
The dna-pk mice live significantly longer compared to ku80-/- mice in both male (p = 0.01) and females (p = 8.7*10-6) mice.Survival of double knock out mice is identical to ku80-/-
Lifespan comparisons
Double mutant dna-pk(CS);ku80(KO) has a lifespan of 230.3 days, while single mutant dna-pk(CS) has a lifespan of 276.5 days and single mutant ku80(KO) has a lifespan of 226.8 days.
Citation
View abstract
Reiling E et al., 2014, The progeroid phenotype of Ku80 deficiency is dominant over DNA-PKCS deficiency. PLoS One. 9(4):e93568 24740260 Click here to select all mutants from this PubMed ID in the graph
Abstract
Ku80 and DNA-PKCS are both involved in the repair of double strand DNA breaks via the nonhomologous end joining (NHEJ) pathway. While ku80-/- mice exhibit a severely reduced lifespan and size, this phenotype is less pronounced in dna-pkcs-/- mice. However, these observations are based on independent studies with varying genetic backgrounds. Here, we generated ku80-/-, dna-pkcs-/- and double knock out mice in a C57Bl6/J*FVB F1 hybrid background and compared their lifespan, end of life pathology and mutation frequency in liver and spleen using a lacZ reporter. Our data confirm that inactivation of Ku80 and DNA-PKCS causes reduced lifespan and bodyweights, which is most severe in ku80-/- mice. All mutant mice exhibited a strong increase in lymphoma incidence as well as other aging-related pathology (skin epidermal and adnexal atrophy, trabacular bone reduction, kidney tubular anisokaryosis, and cortical and medullar atrophy) and severe lymphoid depletion. LacZ mutation frequency analysis did not show strong differences in mutation frequencies between knock out and wild type mice. The ku80-/- mice had the most severe phenotype and the Ku80-mutation was dominant over the DNA-PKCS-mutation. Presumably, the more severe degenerative effect of Ku80 inactivation on lifespan compared to DNA-PKCS inactivation is caused by additional functions of Ku80 or activity of free Ku70 since both Ku80 and DNA-PKCS are essential for NHEJ.

Search genes: Ku80 Prkdc

Symbol
GenAge

Ku80
View on GenAge (Ku80)

No gene information for Ku80

Entrez ID
Symbol
GenAge
MGI ID

19090
Prkdc
View on GenAge (Prkdc)
MGI:104779

protein kinase, DNA activated, catalytic polypeptide

Orthologs of Ku80;Prkdc in SynergyAge

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Not in SynergyAge
Species	Gene

Orthologs of Ku80 in SynergyAge

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Orthologs of Prkdc in SynergyAge

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Species	Gene