hsf-1;rsks-1

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Genetic mutants with hsf-1, rsks-1 alterations

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

Temperature °C
20
Diet
NGM
Lifespan (days)
8.6
Lifespan change (compared to wild type)
-56.78%
Phenotype
The long lifespan of rsks-1(tm1714) mutants was completely suppressed by hsf-1 RNA.
Lifespan comparisons
Double mutant hsf-1(RNAi);rsks-1(tm1714) has a lifespan of 8.6 days, while single mutant hsf-1(RNAi) has a lifespan of 9.2 days, single mutant rsks-1(tm1714) has a lifespan of 23.3 days and wild type has a lifespan of 19.9 days.
Type of interaction
See methods
Opposite lifespan effects of single mutants
Citation
View abstract
Seo K et al., 2013, Heat shock factor 1 mediates the longevity conferred by inhibition of TOR and insulin/IGF-1 signaling pathways in C. elegans. Aging Cell. 12(6):1073-81 23879233 Click here to select all mutants from this PubMed ID in the graph
Abstract
Target of rapamycin (TOR) signaling is an evolutionarily well-conserved pathway that regulates various physiologic processes, including aging and metabolism. One of the key downstream components of TOR signaling is ribosomal protein S6 kinase (S6K) whose inhibition extends the lifespan of yeast, Caenorhabditis elegans, Drosophila, and mice. Here, we demonstrate that the activation of heat shock factor 1 (HSF-1), a crucial longevity transcription factor known to act downstream of the insulin/IGF-1 signaling (IIS) pathway, mediates the prolonged lifespan conferred by mutations in C. elegans S6K (rsks-1). We found that hsf-1 is required for the longevity caused by down-regulation of components in TOR signaling pathways, including TOR and S6K. The induction of a small heat-shock protein hsp-16, a transcriptional target of HSF-1, mediates the long lifespan of rsks-1 mutants. Moreover, we show that synergistic activation of HSF-1 is required for the further enhanced longevity caused by simultaneous down-regulation of TOR and IIS pathways. Our findings suggest that HSF-1 acts as an essential longevity factor that intersects both IIS and TOR signaling pathways.

Temperature °C
22.5
Diet
NGM
Lifespan (days)
5.9
Lifespan change (compared to wild type)
-65.09%
Phenotype
Knockdown of hsf-1 using RNAi only during adulthood completely suppressed the long lifespan of rsks-1 mutants.
Lifespan comparisons
Double mutant hsf-1(RNAi);rsks-1(tm1714) has a lifespan of 5.9 days, while single mutant hsf-1(RNAi) has a lifespan of 11.3 days, single mutant rsks-1(tm1714) has a lifespan of 20.2 days and wild type has a lifespan of 16.9 days.
Type of interaction
See methods
Enhancer, opposite lifespan effects
Citation
View abstract
Seo K et al., 2013, Heat shock factor 1 mediates the longevity conferred by inhibition of TOR and insulin/IGF-1 signaling pathways in C. elegans. Aging Cell. 12(6):1073-81 23879233 Click here to select all mutants from this PubMed ID in the graph
Abstract
Target of rapamycin (TOR) signaling is an evolutionarily well-conserved pathway that regulates various physiologic processes, including aging and metabolism. One of the key downstream components of TOR signaling is ribosomal protein S6 kinase (S6K) whose inhibition extends the lifespan of yeast, Caenorhabditis elegans, Drosophila, and mice. Here, we demonstrate that the activation of heat shock factor 1 (HSF-1), a crucial longevity transcription factor known to act downstream of the insulin/IGF-1 signaling (IIS) pathway, mediates the prolonged lifespan conferred by mutations in C. elegans S6K (rsks-1). We found that hsf-1 is required for the longevity caused by down-regulation of components in TOR signaling pathways, including TOR and S6K. The induction of a small heat-shock protein hsp-16, a transcriptional target of HSF-1, mediates the long lifespan of rsks-1 mutants. Moreover, we show that synergistic activation of HSF-1 is required for the further enhanced longevity caused by simultaneous down-regulation of TOR and IIS pathways. Our findings suggest that HSF-1 acts as an essential longevity factor that intersects both IIS and TOR signaling pathways.

Temperature °C
22.5
Diet
NGM
Lifespan (days)
6.8
Lifespan change (compared to wild type)
-62.64%
Phenotype
Knockdown of hsf-1 using RNAi only during adulthood completely suppressed the long lifespan of rsks-1 mutants.
Lifespan comparisons
Double mutant hsf-1(RNAi);rsks-1(tm1714) has a lifespan of 6.8 days, while single mutant hsf-1(RNAi) has a lifespan of 10.8 days, single mutant rsks-1(tm1714) has a lifespan of 22.3 days and wild type has a lifespan of 18.2 days.
Type of interaction
See methods
Opposite lifespan effects of single mutants
Citation
View abstract
Seo K et al., 2013, Heat shock factor 1 mediates the longevity conferred by inhibition of TOR and insulin/IGF-1 signaling pathways in C. elegans. Aging Cell. 12(6):1073-81 23879233 Click here to select all mutants from this PubMed ID in the graph
Abstract
Target of rapamycin (TOR) signaling is an evolutionarily well-conserved pathway that regulates various physiologic processes, including aging and metabolism. One of the key downstream components of TOR signaling is ribosomal protein S6 kinase (S6K) whose inhibition extends the lifespan of yeast, Caenorhabditis elegans, Drosophila, and mice. Here, we demonstrate that the activation of heat shock factor 1 (HSF-1), a crucial longevity transcription factor known to act downstream of the insulin/IGF-1 signaling (IIS) pathway, mediates the prolonged lifespan conferred by mutations in C. elegans S6K (rsks-1). We found that hsf-1 is required for the longevity caused by down-regulation of components in TOR signaling pathways, including TOR and S6K. The induction of a small heat-shock protein hsp-16, a transcriptional target of HSF-1, mediates the long lifespan of rsks-1 mutants. Moreover, we show that synergistic activation of HSF-1 is required for the further enhanced longevity caused by simultaneous down-regulation of TOR and IIS pathways. Our findings suggest that HSF-1 acts as an essential longevity factor that intersects both IIS and TOR signaling pathways.

Temperature °C
22.5
Diet
NGM
Lifespan (days)
10.5
Lifespan change (compared to wild type)
-41.01%
Phenotype
hsf-1 RNAi treatment only during adulthood (adult-only RNAi) suppressed the longevity of rsks-1(tm1714) mutants.
Lifespan comparisons
Double mutant hsf-1(RNAi);rsks-1(tm1714) has a lifespan of 10.5 days, while single mutant hsf-1(RNAi) has a lifespan of 10.3 days, single mutant rsks-1(tm1714) has a lifespan of 21.4 days and wild type has a lifespan of 17.8 days.
Type of interaction
See methods
Opposite lifespan effects of single mutants
Citation
View abstract
Seo K et al., 2013, Heat shock factor 1 mediates the longevity conferred by inhibition of TOR and insulin/IGF-1 signaling pathways in C. elegans. Aging Cell. 12(6):1073-81 23879233 Click here to select all mutants from this PubMed ID in the graph
Abstract
Target of rapamycin (TOR) signaling is an evolutionarily well-conserved pathway that regulates various physiologic processes, including aging and metabolism. One of the key downstream components of TOR signaling is ribosomal protein S6 kinase (S6K) whose inhibition extends the lifespan of yeast, Caenorhabditis elegans, Drosophila, and mice. Here, we demonstrate that the activation of heat shock factor 1 (HSF-1), a crucial longevity transcription factor known to act downstream of the insulin/IGF-1 signaling (IIS) pathway, mediates the prolonged lifespan conferred by mutations in C. elegans S6K (rsks-1). We found that hsf-1 is required for the longevity caused by down-regulation of components in TOR signaling pathways, including TOR and S6K. The induction of a small heat-shock protein hsp-16, a transcriptional target of HSF-1, mediates the long lifespan of rsks-1 mutants. Moreover, we show that synergistic activation of HSF-1 is required for the further enhanced longevity caused by simultaneous down-regulation of TOR and IIS pathways. Our findings suggest that HSF-1 acts as an essential longevity factor that intersects both IIS and TOR signaling pathways.

Temperature °C
22.5
Diet
NGM
Lifespan (days)
6.9
Lifespan change (compared to wild type)
-57.41%
Phenotype
hsf-1 RNAi treatment only during adulthood (adult-only RNAi) suppressed the longevity of rsks-1(tm1714) mutants.
Lifespan comparisons
Double mutant hsf-1(RNAi);rsks-1(tm1714) has a lifespan of 6.9 days, while single mutant hsf-1(RNAi) has a lifespan of 7.6 days, single mutant rsks-1(tm1714) has a lifespan of 18.5 days and wild type has a lifespan of 16.2 days.
Type of interaction
See methods
Opposite lifespan effects of single mutants
Citation
View abstract
Seo K et al., 2013, Heat shock factor 1 mediates the longevity conferred by inhibition of TOR and insulin/IGF-1 signaling pathways in C. elegans. Aging Cell. 12(6):1073-81 23879233 Click here to select all mutants from this PubMed ID in the graph
Abstract
Target of rapamycin (TOR) signaling is an evolutionarily well-conserved pathway that regulates various physiologic processes, including aging and metabolism. One of the key downstream components of TOR signaling is ribosomal protein S6 kinase (S6K) whose inhibition extends the lifespan of yeast, Caenorhabditis elegans, Drosophila, and mice. Here, we demonstrate that the activation of heat shock factor 1 (HSF-1), a crucial longevity transcription factor known to act downstream of the insulin/IGF-1 signaling (IIS) pathway, mediates the prolonged lifespan conferred by mutations in C. elegans S6K (rsks-1). We found that hsf-1 is required for the longevity caused by down-regulation of components in TOR signaling pathways, including TOR and S6K. The induction of a small heat-shock protein hsp-16, a transcriptional target of HSF-1, mediates the long lifespan of rsks-1 mutants. Moreover, we show that synergistic activation of HSF-1 is required for the further enhanced longevity caused by simultaneous down-regulation of TOR and IIS pathways. Our findings suggest that HSF-1 acts as an essential longevity factor that intersects both IIS and TOR signaling pathways.

Temperature °C
20
Diet
NGM
Lifespan (days)
7.2
Lifespan change (compared to wild type)
-63.45%
Lifespan comparisons
Double mutant hsf-1(RNAi);rsks-1(tm1714) has a lifespan of 7.2 days, while single mutant hsf-1(RNAi) has a lifespan of 9.9 days, single mutant rsks-1(tm1714) has a lifespan of 21.0 days and wild type has a lifespan of 19.7 days.
Type of interaction
See methods
Enhancer, opposite lifespan effects
Citation
View abstract
Seo K et al., 2013, Heat shock factor 1 mediates the longevity conferred by inhibition of TOR and insulin/IGF-1 signaling pathways in C. elegans. Aging Cell. 12(6):1073-81 23879233 Click here to select all mutants from this PubMed ID in the graph
Abstract
Target of rapamycin (TOR) signaling is an evolutionarily well-conserved pathway that regulates various physiologic processes, including aging and metabolism. One of the key downstream components of TOR signaling is ribosomal protein S6 kinase (S6K) whose inhibition extends the lifespan of yeast, Caenorhabditis elegans, Drosophila, and mice. Here, we demonstrate that the activation of heat shock factor 1 (HSF-1), a crucial longevity transcription factor known to act downstream of the insulin/IGF-1 signaling (IIS) pathway, mediates the prolonged lifespan conferred by mutations in C. elegans S6K (rsks-1). We found that hsf-1 is required for the longevity caused by down-regulation of components in TOR signaling pathways, including TOR and S6K. The induction of a small heat-shock protein hsp-16, a transcriptional target of HSF-1, mediates the long lifespan of rsks-1 mutants. Moreover, we show that synergistic activation of HSF-1 is required for the further enhanced longevity caused by simultaneous down-regulation of TOR and IIS pathways. Our findings suggest that HSF-1 acts as an essential longevity factor that intersects both IIS and TOR signaling pathways.

Temperature °C
20
Diet
NGM
Lifespan (days)
7.8
Lifespan change (compared to wild type)
-58.73%
Lifespan comparisons
Double mutant hsf-1(RNAi);rsks-1(tm1714) has a lifespan of 7.8 days, while single mutant hsf-1(RNAi) has a lifespan of 11.2 days, single mutant rsks-1(tm1714) has a lifespan of 20.1 days and wild type has a lifespan of 18.9 days.
Type of interaction
See methods
Enhancer, opposite lifespan effects
Citation
View abstract
Seo K et al., 2013, Heat shock factor 1 mediates the longevity conferred by inhibition of TOR and insulin/IGF-1 signaling pathways in C. elegans. Aging Cell. 12(6):1073-81 23879233 Click here to select all mutants from this PubMed ID in the graph
Abstract
Target of rapamycin (TOR) signaling is an evolutionarily well-conserved pathway that regulates various physiologic processes, including aging and metabolism. One of the key downstream components of TOR signaling is ribosomal protein S6 kinase (S6K) whose inhibition extends the lifespan of yeast, Caenorhabditis elegans, Drosophila, and mice. Here, we demonstrate that the activation of heat shock factor 1 (HSF-1), a crucial longevity transcription factor known to act downstream of the insulin/IGF-1 signaling (IIS) pathway, mediates the prolonged lifespan conferred by mutations in C. elegans S6K (rsks-1). We found that hsf-1 is required for the longevity caused by down-regulation of components in TOR signaling pathways, including TOR and S6K. The induction of a small heat-shock protein hsp-16, a transcriptional target of HSF-1, mediates the long lifespan of rsks-1 mutants. Moreover, we show that synergistic activation of HSF-1 is required for the further enhanced longevity caused by simultaneous down-regulation of TOR and IIS pathways. Our findings suggest that HSF-1 acts as an essential longevity factor that intersects both IIS and TOR signaling pathways.

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

Temperature °C
22.5
Diet
NGM
Lifespan (days)
14.5
Lifespan change (compared to wild type)
-25.26%
Phenotype
The long lifespan of rsks-1(tm1714) mutants was completely suppressed by hsf-1(sy441) mutations.
Lifespan comparisons
Double mutant hsf-1(sy441);rsks-1(tm1714) has a lifespan of 14.5 days, while single mutant rsks-1(tm1714) has a lifespan of 22.4 days, single mutant hsf-1(sy441) has a lifespan of 14.3 days and wild type has a lifespan of 19.4 days.
Type of interaction
See methods
Opposite lifespan effects of single mutants
Citation
View abstract
Seo K et al., 2013, Heat shock factor 1 mediates the longevity conferred by inhibition of TOR and insulin/IGF-1 signaling pathways in C. elegans. Aging Cell. 12(6):1073-81 23879233 Click here to select all mutants from this PubMed ID in the graph
Abstract
Target of rapamycin (TOR) signaling is an evolutionarily well-conserved pathway that regulates various physiologic processes, including aging and metabolism. One of the key downstream components of TOR signaling is ribosomal protein S6 kinase (S6K) whose inhibition extends the lifespan of yeast, Caenorhabditis elegans, Drosophila, and mice. Here, we demonstrate that the activation of heat shock factor 1 (HSF-1), a crucial longevity transcription factor known to act downstream of the insulin/IGF-1 signaling (IIS) pathway, mediates the prolonged lifespan conferred by mutations in C. elegans S6K (rsks-1). We found that hsf-1 is required for the longevity caused by down-regulation of components in TOR signaling pathways, including TOR and S6K. The induction of a small heat-shock protein hsp-16, a transcriptional target of HSF-1, mediates the long lifespan of rsks-1 mutants. Moreover, we show that synergistic activation of HSF-1 is required for the further enhanced longevity caused by simultaneous down-regulation of TOR and IIS pathways. Our findings suggest that HSF-1 acts as an essential longevity factor that intersects both IIS and TOR signaling pathways.

Temperature °C
22.5
Diet
NGM
Lifespan (days)
14.7
Lifespan change (compared to wild type)
-27.23%
Phenotype
The long lifespan of rsks-1(tm1714) mutants was completely suppressed by hsf-1(sy441) mutations.
Lifespan comparisons
Double mutant hsf-1(sy441);rsks-1(tm1714) has a lifespan of 14.7 days, while single mutant rsks-1(tm1714) has a lifespan of 25.2 days, single mutant hsf-1(sy441) has a lifespan of 14.7 days and wild type has a lifespan of 20.2 days.
Type of interaction
See methods
Opposite lifespan effects of single mutants
Citation
View abstract
Seo K et al., 2013, Heat shock factor 1 mediates the longevity conferred by inhibition of TOR and insulin/IGF-1 signaling pathways in C. elegans. Aging Cell. 12(6):1073-81 23879233 Click here to select all mutants from this PubMed ID in the graph
Abstract
Target of rapamycin (TOR) signaling is an evolutionarily well-conserved pathway that regulates various physiologic processes, including aging and metabolism. One of the key downstream components of TOR signaling is ribosomal protein S6 kinase (S6K) whose inhibition extends the lifespan of yeast, Caenorhabditis elegans, Drosophila, and mice. Here, we demonstrate that the activation of heat shock factor 1 (HSF-1), a crucial longevity transcription factor known to act downstream of the insulin/IGF-1 signaling (IIS) pathway, mediates the prolonged lifespan conferred by mutations in C. elegans S6K (rsks-1). We found that hsf-1 is required for the longevity caused by down-regulation of components in TOR signaling pathways, including TOR and S6K. The induction of a small heat-shock protein hsp-16, a transcriptional target of HSF-1, mediates the long lifespan of rsks-1 mutants. Moreover, we show that synergistic activation of HSF-1 is required for the further enhanced longevity caused by simultaneous down-regulation of TOR and IIS pathways. Our findings suggest that HSF-1 acts as an essential longevity factor that intersects both IIS and TOR signaling pathways.

Search genes: hsf-1 rsks-1

Entrez ID
Symbol
GenAge
Wormbase ID

173078
hsf-1
View on GenAge (hsf-1)
WBGene00002004

Heat Shock Factor

Locus: CELE_Y53C10A.12

Wormbase description: hsf-1 encodes the C. elegans heat-shock transcription factor ortholog; HSF-1 functions as a transcriptional regulator of stress-induced gene expression whose activity is required for heat-shock and proteotoxicity response, larval development, innate immunity, and regulation of adult lifespan; HSF-1 binds bovine calmodulin in vitro in a calcium-dependent manner.

Entrez ID
Symbol
GenAge
Wormbase ID

176554
rsks-1
View on GenAge (rsks-1)
WBGene00012929

Ribosomal protein S6 kinase beta

Locus: CELE_Y47D3A.16

Wormbase description: rsks-1 encodes a putative ribosomal protein S6 kinase (S6K) required additively with IFG-1 for normally high levels of protein synthesis, and for normally short lifespan; RSKS-1's effect on lifespan is independent of DAF-16, ISP-1, and SIR-2.1, and does not correlate with juglone resistance, but does correlate with abnormally high resistance to starvation and (perhaps) thermotolerance; RSKS-1 is required for normal juglone resistance, as well as normally rapid growth and normal brood sizes; RSKS-1 is expressed in E-lineage embryonic cells, and in pharyngeal and hypodermal cells of larvae and adults; RSKS-1 is orthologous to human RPS6KB1 (OMIM:608938) and RPS6KB2 (OMIM:608939).

Orthologs of hsf-1;rsks-1 in SynergyAge

Show in SynergyAge
Species	Gene

Not in SynergyAge
Species	Gene

Orthologs of hsf-1 in SynergyAge

Show in SynergyAge
Species	Gene

Orthologs of rsks-1 in SynergyAge

Show in SynergyAge
Species	Gene

Not in SynergyAge
Species	Gene
Drosophila melanogaster	S6k
Mus musculus	Rps6kb1
Mus musculus	Rps6kb2