clk-1;clk-2

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Genetic mutants with clk-1, clk-2 alterations

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

Temperature °C
18
Lifespan (days)
28.2
Lifespan change (compared to wild type)
89.26%
Phenotype
The mean life-span of clk-1(e2519) clk-2(qm37) mutants is more than 50% greater than that of either clk-l (e2519) or clk-2(qm37) alone and almost 90% greater than that of the wild type.
Lifespan comparisons
Double mutant clk-1(e2519);clk-2(qm37) has a lifespan of 28.2 days, while single mutant clk-2(qm37) has a lifespan of 18.7 days, single mutant clk-1(e2519) has a lifespan of 18.4 days and wild type has a lifespan of 14.9 days.
Type of interaction
See methods
Synergistic (positive)
Citation
View abstract
Lakowski B, Hekimi S, 1996, Determination of life-span in Caenorhabditis elegans by four clock genes. Science. 272(5264):1010-3 8638122 Click here to select all mutants from this PubMed ID in the graph
Abstract
The nematode worm Caenorhabditis elegans is a model system for the study of the genetic basis of aging. Maternal-effect mutations in four genes--clk-1, clk-2, clk-3, and gro-1--interact genetically to determine both the duration of development and life-span. Analysis of the phenotypes of these mutants suggests the existence of a general physiological clock in the worm. Mutations in certain genes involved in dauer formation (an alternative larval stage induced by adverse conditions in which development is arrested) can also extend life-span, but the life extension of Clock mutants appears to be independent of these genes. The daf-2(e1370) clk-1(e2519) worms, which carry life-span-extending mutations from two different pathways, live nearly five times as long as wild-type worms.

Temperature °C
20
Lifespan (days)
23.1
Lifespan change (compared to wild type)
43.48%
Lifespan comparisons
Double mutant clk-1(e2519);clk-2(qm37) has a lifespan of 23.1 days, while single mutant clk-2(qm37) has a lifespan of 18.0 days, single mutant clk-1(e2519) has a lifespan of 17.3 days and wild type has a lifespan of 16.1 days.
Type of interaction
See methods
Synergistic (positive)
Citation
View abstract
Lakowski B, Hekimi S, 1996, Determination of life-span in Caenorhabditis elegans by four clock genes. Science. 272(5264):1010-3 8638122 Click here to select all mutants from this PubMed ID in the graph
Abstract
The nematode worm Caenorhabditis elegans is a model system for the study of the genetic basis of aging. Maternal-effect mutations in four genes--clk-1, clk-2, clk-3, and gro-1--interact genetically to determine both the duration of development and life-span. Analysis of the phenotypes of these mutants suggests the existence of a general physiological clock in the worm. Mutations in certain genes involved in dauer formation (an alternative larval stage induced by adverse conditions in which development is arrested) can also extend life-span, but the life extension of Clock mutants appears to be independent of these genes. The daf-2(e1370) clk-1(e2519) worms, which carry life-span-extending mutations from two different pathways, live nearly five times as long as wild-type worms.

Temperature °C
15
Lifespan (days)
34.5
Lifespan change (compared to wild type)
56.82%
Lifespan comparisons
Double mutant clk-1(e2519);clk-2(qm37) has a lifespan of 34.5 days, while single mutant clk-2(qm37) has a lifespan of 24.6 days, single mutant clk-1(e2519) has a lifespan of 29.3 days and wild type has a lifespan of 22.0 days.
Type of interaction
See methods
Partially known monotony. Positive epistasis
Citation
View abstract
Lakowski B, Hekimi S, 1996, Determination of life-span in Caenorhabditis elegans by four clock genes. Science. 272(5264):1010-3 8638122 Click here to select all mutants from this PubMed ID in the graph
Abstract
The nematode worm Caenorhabditis elegans is a model system for the study of the genetic basis of aging. Maternal-effect mutations in four genes--clk-1, clk-2, clk-3, and gro-1--interact genetically to determine both the duration of development and life-span. Analysis of the phenotypes of these mutants suggests the existence of a general physiological clock in the worm. Mutations in certain genes involved in dauer formation (an alternative larval stage induced by adverse conditions in which development is arrested) can also extend life-span, but the life extension of Clock mutants appears to be independent of these genes. The daf-2(e1370) clk-1(e2519) worms, which carry life-span-extending mutations from two different pathways, live nearly five times as long as wild-type worms.

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

Temperature °C
18
Lifespan (days)
28.3
Lifespan change (compared to wild type)
89.93%
Phenotype
The mean life-span of clk-1(qm30) clk-2(qm37) mutants is more than 50% greater than that of either clk-l (e2519) or clk-2(qm37) alone and almost 90% greater than that of the wild type.
Lifespan comparisons
Double mutant clk-1(qm30);clk-2(qm37) has a lifespan of 28.3 days, while single mutant clk-2(qm37) has a lifespan of 18.7 days, single mutant clk-1(qm30) has a lifespan of 19.8 days and wild type has a lifespan of 14.9 days.
Type of interaction
See methods
Synergistic (positive)
Citation
View abstract
Lakowski B, Hekimi S, 1996, Determination of life-span in Caenorhabditis elegans by four clock genes. Science. 272(5264):1010-3 8638122 Click here to select all mutants from this PubMed ID in the graph
Abstract
The nematode worm Caenorhabditis elegans is a model system for the study of the genetic basis of aging. Maternal-effect mutations in four genes--clk-1, clk-2, clk-3, and gro-1--interact genetically to determine both the duration of development and life-span. Analysis of the phenotypes of these mutants suggests the existence of a general physiological clock in the worm. Mutations in certain genes involved in dauer formation (an alternative larval stage induced by adverse conditions in which development is arrested) can also extend life-span, but the life extension of Clock mutants appears to be independent of these genes. The daf-2(e1370) clk-1(e2519) worms, which carry life-span-extending mutations from two different pathways, live nearly five times as long as wild-type worms.

Temperature °C
20
Lifespan (days)
25.4
Lifespan change (compared to wild type)
57.76%
Lifespan comparisons
Double mutant clk-1(qm30);clk-2(qm37) has a lifespan of 25.4 days, while single mutant clk-2(qm37) has a lifespan of 18.0 days, single mutant clk-1(qm30) has a lifespan of 19.3 days and wild type has a lifespan of 16.1 days.
Type of interaction
See methods
Synergistic (positive)
Citation
View abstract
Lakowski B, Hekimi S, 1996, Determination of life-span in Caenorhabditis elegans by four clock genes. Science. 272(5264):1010-3 8638122 Click here to select all mutants from this PubMed ID in the graph
Abstract
The nematode worm Caenorhabditis elegans is a model system for the study of the genetic basis of aging. Maternal-effect mutations in four genes--clk-1, clk-2, clk-3, and gro-1--interact genetically to determine both the duration of development and life-span. Analysis of the phenotypes of these mutants suggests the existence of a general physiological clock in the worm. Mutations in certain genes involved in dauer formation (an alternative larval stage induced by adverse conditions in which development is arrested) can also extend life-span, but the life extension of Clock mutants appears to be independent of these genes. The daf-2(e1370) clk-1(e2519) worms, which carry life-span-extending mutations from two different pathways, live nearly five times as long as wild-type worms.

Temperature °C
15
Lifespan (days)
30.3
Lifespan change (compared to wild type)
37.73%
Lifespan comparisons
Double mutant clk-1(qm30);clk-2(qm37) has a lifespan of 30.3 days, while single mutant clk-2(qm37) has a lifespan of 24.6 days, single mutant clk-1(qm30) has a lifespan of 31.0 days and wild type has a lifespan of 22.0 days.
Type of interaction
See methods
Contains dependence
Citation
View abstract
Lakowski B, Hekimi S, 1996, Determination of life-span in Caenorhabditis elegans by four clock genes. Science. 272(5264):1010-3 8638122 Click here to select all mutants from this PubMed ID in the graph
Abstract
The nematode worm Caenorhabditis elegans is a model system for the study of the genetic basis of aging. Maternal-effect mutations in four genes--clk-1, clk-2, clk-3, and gro-1--interact genetically to determine both the duration of development and life-span. Analysis of the phenotypes of these mutants suggests the existence of a general physiological clock in the worm. Mutations in certain genes involved in dauer formation (an alternative larval stage induced by adverse conditions in which development is arrested) can also extend life-span, but the life extension of Clock mutants appears to be independent of these genes. The daf-2(e1370) clk-1(e2519) worms, which carry life-span-extending mutations from two different pathways, live nearly five times as long as wild-type worms.

Search genes: clk-1 clk-2

Entrez ID
Symbol
GenAge
Wormbase ID

175729
clk-1
View on GenAge (clk-1)
WBGene00000536

5-demethoxyubiquinone hydroxylase, mitochondrial

Locus: CELE_ZC395.2

Wormbase description: clk-1 encodes the C. elegans ortholog of COQ7/CAT5, a highly conserved demethoxyubiquinone (DMQ) hydroxylase that is necessary for the biosynthesis of ubiquinone (coenzyme Q, Q9) from 5-demethoxyubiquinone (DMQ9); in C. elegans, CLK-1 activity is required for normal physiological rates of growth, development, behavior, and aging, as well as for normal brood sizes.

Entrez ID
Symbol
GenAge
Wormbase ID

176065
clk-2
View on GenAge (clk-2)
WBGene00000537

Telomere length regulation protein clk-2

Locus: CELE_C07H6.6

Wormbase description: The clk-2 gene encodes an ortholog of the S. cerevisiae telomere length-regulating protein Tel2p that has been shown to bind a number of DNA structures in vitro, including single-, double- and four-stranded DNA; in C. elegans, CLK-2 activity is required for the DNA damage and S phase replication checkpoints, for embryonic development, and for normal biological rhythms and life span; a functional CLK-2::GFP fusion protein is detected exclusively in the cytoplasm of somatic tissues.

Orthologs of clk-1;clk-2 in SynergyAge

Show in SynergyAge
Species	Gene

Not in SynergyAge
Species	Gene
Mus musculus	Coq7;Telo2

Orthologs of clk-1 in SynergyAge

Show in SynergyAge
Species	Gene

Not in SynergyAge
Species	Gene
Drosophila melanogaster	COQ7
Mus musculus	Coq7

Orthologs of clk-2 in SynergyAge

Show in SynergyAge
Species	Gene

Not in SynergyAge
Species	Gene
Mus musculus	Telo2