fem-1;fer-15;rsks-1

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Genetic mutants with fem-1, fer-15, rsks-1 alterations

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

Temperature °C
20
Lifespan (days)
24.8
Phenotype
These RNAi treatments reduced RP mRNA levels approximately two- to fivefold and, in each case, increased lifespan significantly.
Lifespan comparisons
Triple mutant fem-1(hc17);fer-15(b26);rsks-1(RNAi) has a lifespan of 24.8 days, while double mutant fem-1(hc17);fer-15(b26) has a lifespan of 21.9 days.
Citation
View abstract
Hansen M et al., 2007, Lifespan extension by conditions that inhibit translation in Caenorhabditis elegans. Aging Cell. 6(1):95-110 17266679 Click here to select all mutants from this PubMed ID in the graph
Abstract
Many conditions that shift cells from states of nutrient utilization and growth to states of cell maintenance extend lifespan. We have carried out a systematic lifespan analysis of conditions that inhibit protein synthesis. We find that reducing the levels of ribosomal proteins, ribosomal-protein S6 kinase or translation-initiation factors increases the lifespan of Caenorhabditis elegans. These perturbations, as well as inhibition of the nutrient sensor target of rapamycin (TOR), which is known to increase lifespan, all increase thermal-stress resistance. Thus inhibiting translation may extend lifespan by shifting cells to physiological states that favor maintenance and repair. Interestingly, different types of translation inhibition lead to one of two mutually exclusive outputs, one that increases lifespan and stress resistance through the transcription factor DAF-16/FOXO, and one that increases lifespan and stress resistance independently of DAF-16. Our findings link TOR, but not sir-2.1, to the longevity response induced by dietary restriction (DR) in C. elegans, and they suggest that neither TOR inhibition nor DR extends lifespan simply by reducing protein synthesis.

Temperature °C
20
Lifespan (days)
25.3
Phenotype
These RNAi treatments reduced RP mRNA levels approximately two- to fivefold and, in each case, increased lifespan significantly.
Lifespan comparisons
Triple mutant fem-1(hc17);fer-15(b26);rsks-1(RNAi) has a lifespan of 25.3 days, while double mutant fem-1(hc17);fer-15(b26) has a lifespan of 22.4 days.
Citation
View abstract
Hansen M et al., 2007, Lifespan extension by conditions that inhibit translation in Caenorhabditis elegans. Aging Cell. 6(1):95-110 17266679 Click here to select all mutants from this PubMed ID in the graph
Abstract
Many conditions that shift cells from states of nutrient utilization and growth to states of cell maintenance extend lifespan. We have carried out a systematic lifespan analysis of conditions that inhibit protein synthesis. We find that reducing the levels of ribosomal proteins, ribosomal-protein S6 kinase or translation-initiation factors increases the lifespan of Caenorhabditis elegans. These perturbations, as well as inhibition of the nutrient sensor target of rapamycin (TOR), which is known to increase lifespan, all increase thermal-stress resistance. Thus inhibiting translation may extend lifespan by shifting cells to physiological states that favor maintenance and repair. Interestingly, different types of translation inhibition lead to one of two mutually exclusive outputs, one that increases lifespan and stress resistance through the transcription factor DAF-16/FOXO, and one that increases lifespan and stress resistance independently of DAF-16. Our findings link TOR, but not sir-2.1, to the longevity response induced by dietary restriction (DR) in C. elegans, and they suggest that neither TOR inhibition nor DR extends lifespan simply by reducing protein synthesis.

Search genes: fem-1 fer-15 rsks-1 fem-1;fer-15;rsks-1

Entrez ID
Symbol
GenAge
Wormbase ID

177335
fem-1
View on GenAge (fem-1)
WBGene00001411

Sex-determining protein fem-1

Locus: CELE_F35D6.1

Wormbase description: The fem-1 gene encodes an ankyrin repeat-containing protein orthologous to human FEM1A and is required for masculinization of germline and somatic tissues; FEM-1 is widely expressed and functions as a second messenger in the sex determination pathway, connecting the membrane protein TRA-2A to the transcription factor TRA-1A which it negatively regulates; FEM-1 may also play a role in apoptosis, as it is a substrate for the CED-3 protease and can induce apoptosis when overexpressed in mammalian cells.

Symbol
GenAge

fer-15
View on GenAge (fer-15)

No gene information for fer-15

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 fem-1;fer-15;rsks-1 in SynergyAge

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Species	Gene

Not in SynergyAge
Species	Gene

Orthologs of fem-1 in SynergyAge

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Species	Gene

Orthologs of fer-15 in SynergyAge

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Species	Gene

Orthologs of rsks-1 in SynergyAge

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Species	Gene

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