fem-1;fer-15;ifg-1

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

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

Temperature °C
20
Lifespan (days)
33.1
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);ifg-1(RNAi) has a lifespan of 33.1 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.

Temperature °C
20
Lifespan (days)
28.5
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);ifg-1(RNAi) has a lifespan of 28.5 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)
24.9
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);ifg-1(RNAi) has a lifespan of 24.9 days, while double mutant fem-1(hc17);fer-15(b26) has a lifespan of 22.8 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 ifg-1 fem-1;fer-15;ifg-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

174322
ifg-1
View on GenAge (ifg-1)
WBGene00002066

Initiation Factor 4G (eIF4G) family

Locus: CELE_M110.4

Wormbase description: ifg-1 encodes, by alternative splicing, two orthologs of the translation initiation factor 4F, ribosome/mRNA-bridging subunit (eIF-4G); by homology, IFG-1 is predicted to function in poly(A) tail-dependent translation initiation; loss of ifg-1 activity in adult animals extends lifespan.

Orthologs of fem-1;fer-15;ifg-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 ifg-1 in SynergyAge

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Species	Gene

Not in SynergyAge
Species	Gene
Drosophila melanogaster	eIF4G2
Mus musculus	Eif4g1
Mus musculus	Eif4g3