Atm;Terc

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Genetic mutants with Atm, Terc alterations

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

Lifespan (days)
380.0
Lifespan change (compared to wild type)
-37.70%
Phenotype
Despite cancer resistance, the median lifespan of the G3/G4 Terc-/- Atm-/- mice was significantly shorter than that of G3/G4 Terc-/- Atm+/+ controls
Lifespan comparisons
Double mutant Terc(KO);atm(KO) has a lifespan of 380.0 days, while single mutant atm(KO) has a lifespan of 395.0 days, single mutant Terc(KO) has a lifespan of 610.0 days and wild type has a lifespan of 610.0 days.
Type of interaction
See methods
Synergistic (negative)
Citation
View abstract
Wong KK et al., 2003, Telomere dysfunction and Atm deficiency compromises organ homeostasis and accelerates ageing. Nature. 421(6923):643-8 12540856 Click here to select all mutants from this PubMed ID in the graph
Abstract
Ataxia-telangiectasia (A-T) results from the loss of ataxia-telangiectasia mutated (Atm) function and is characterized by accelerated telomere loss, genomic instability, progressive neurological degeneration, premature ageing and increased neoplasia incidence. Here we evaluate the functional interaction of Atm and telomeres in vivo. We examined the impact of Atm deficiency as a function of progressive telomere attrition at both the cellular and whole-organism level in mice doubly null for Atm and the telomerase RNA component (Terc). These compound mutants showed increased telomere erosion and genomic instability, yet they experienced a substantial elimination of T-cell lymphomas associated with Atm deficiency. A generalized proliferation defect was evident in all cell types and tissues examined, and this defect extended to tissue stem/progenitor cell compartments, thereby providing a basis for progressive multi-organ system compromise, accelerated ageing and premature death. We show that Atm deficiency and telomere dysfunction act together to impair cellular and whole-organism viability, thus supporting the view that aspects of A-T pathophysiology are linked to the functional state of telomeres and its adverse effects on stem/progenitor cell reserves.

Lifespan (days)
380.0
Lifespan change (compared to wild type)
-37.70%
Phenotype
Despite cancer resistance, the median lifespan of the G3/G4 Terc-/- Atm-/- mice was significantly shorter than that of G3/G4 Terc-/- Atm+/+ controls
Lifespan comparisons
Double mutant atm(KO);Terc(KO) has a lifespan of 380.0 days, while single mutant atm(KO) has a lifespan of 395.0 days, single mutant Terc(KO) has a lifespan of 610.0 days and wild type has a lifespan of 610.0 days.
Type of interaction
See methods
Synergistic (negative)
Citation
View abstract
Wong KK et al., 2003, Telomere dysfunction and Atm deficiency compromises organ homeostasis and accelerates ageing. Nature. 421(6923):643-8 12540856 Click here to select all mutants from this PubMed ID in the graph
Abstract
Ataxia-telangiectasia (A-T) results from the loss of ataxia-telangiectasia mutated (Atm) function and is characterized by accelerated telomere loss, genomic instability, progressive neurological degeneration, premature ageing and increased neoplasia incidence. Here we evaluate the functional interaction of Atm and telomeres in vivo. We examined the impact of Atm deficiency as a function of progressive telomere attrition at both the cellular and whole-organism level in mice doubly null for Atm and the telomerase RNA component (Terc). These compound mutants showed increased telomere erosion and genomic instability, yet they experienced a substantial elimination of T-cell lymphomas associated with Atm deficiency. A generalized proliferation defect was evident in all cell types and tissues examined, and this defect extended to tissue stem/progenitor cell compartments, thereby providing a basis for progressive multi-organ system compromise, accelerated ageing and premature death. We show that Atm deficiency and telomere dysfunction act together to impair cellular and whole-organism viability, thus supporting the view that aspects of A-T pathophysiology are linked to the functional state of telomeres and its adverse effects on stem/progenitor cell reserves.

Search genes: Atm Terc

Entrez ID
Symbol
GenAge
MGI ID

11920
Atm
View on GenAge (Atm)
MGI:107202

ataxia telangiectasia mutated

Entrez ID
Symbol
GenAge
MGI ID

21748
Terc
View on GenAge (Terc)
MGI:109558

telomerase RNA component

Orthologs of Atm;Terc in SynergyAge

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Species	Gene

Not in SynergyAge
Species	Gene

Orthologs of Atm in SynergyAge

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Species	Gene

Not in SynergyAge
Species	Gene
Drosophila melanogaster	tefu

Orthologs of Terc in SynergyAge

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Species	Gene