bec-1;eat-2;rrf-3

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Genetic mutants with bec-1, eat-2, rrf-3 alterations

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

Temperature °C
20
Diet
OP50
Lifespan (days)
17.0
Lifespan comparisons
Triple mutant bec-1(RNAi);eat-2(ad1116);rrf-3(pk1426) has a lifespan of 17.0 days, while double mutant eat-2(ad1116);rrf-3(pk1426) has a lifespan of 19.3 days.
Type of interaction
See methods
Contains dependence
Citation
View abstract
Hansen M et al., 2008, A role for autophagy in the extension of lifespan by dietary restriction in C. elegans. PLoS Genet. 4(2):e24 18282106 Click here to select all mutants from this PubMed ID in the graph
Abstract
In many organisms, dietary restriction appears to extend lifespan, at least in part, by down-regulating the nutrient-sensor TOR (Target Of Rapamycin). TOR inhibition elicits autophagy, the large-scale recycling of cytoplasmic macromolecules and organelles. In this study, we asked whether autophagy might contribute to the lifespan extension induced by dietary restriction in C. elegans. We find that dietary restriction and TOR inhibition produce an autophagic phenotype and that inhibiting genes required for autophagy prevents dietary restriction and TOR inhibition from extending lifespan. The longevity response to dietary restriction in C. elegans requires the PHA-4 transcription factor. We find that the autophagic response to dietary restriction also requires PHA-4 activity, indicating that autophagy is a transcriptionally regulated response to food limitation. In spite of the rejuvenating effect that autophagy is predicted to have on cells, our findings suggest that autophagy is not sufficient to extend lifespan. Long-lived daf-2 insulin/IGF-1 receptor mutants require both autophagy and the transcription factor DAF-16/FOXO for their longevity, but we find that autophagy takes place in the absence of DAF-16. Perhaps autophagy is not sufficient for lifespan extension because although it provides raw material for new macromolecular synthesis, DAF-16/FOXO must program the cells to recycle this raw material into cell-protective longevity proteins.

Temperature °C
20
Diet
OP50
Lifespan (days)
15.9
Lifespan change (compared to wild type)
-19.29%
Lifespan comparisons
Triple mutant bec-1(RNAi);eat-2(ad1116);rrf-3(pk1426) has a lifespan of 15.9 days, while single mutant bec-1(RNAi) has a lifespan of 19.8 days, double mutant eat-2(ad1116);rrf-3(pk1426) has a lifespan of 19.3 days and wild type has a lifespan of 19.8 days.
Type of interaction
See methods
Contains dependence
Citation
View abstract
Hansen M et al., 2008, A role for autophagy in the extension of lifespan by dietary restriction in C. elegans. PLoS Genet. 4(2):e24 18282106 Click here to select all mutants from this PubMed ID in the graph
Abstract
In many organisms, dietary restriction appears to extend lifespan, at least in part, by down-regulating the nutrient-sensor TOR (Target Of Rapamycin). TOR inhibition elicits autophagy, the large-scale recycling of cytoplasmic macromolecules and organelles. In this study, we asked whether autophagy might contribute to the lifespan extension induced by dietary restriction in C. elegans. We find that dietary restriction and TOR inhibition produce an autophagic phenotype and that inhibiting genes required for autophagy prevents dietary restriction and TOR inhibition from extending lifespan. The longevity response to dietary restriction in C. elegans requires the PHA-4 transcription factor. We find that the autophagic response to dietary restriction also requires PHA-4 activity, indicating that autophagy is a transcriptionally regulated response to food limitation. In spite of the rejuvenating effect that autophagy is predicted to have on cells, our findings suggest that autophagy is not sufficient to extend lifespan. Long-lived daf-2 insulin/IGF-1 receptor mutants require both autophagy and the transcription factor DAF-16/FOXO for their longevity, but we find that autophagy takes place in the absence of DAF-16. Perhaps autophagy is not sufficient for lifespan extension because although it provides raw material for new macromolecular synthesis, DAF-16/FOXO must program the cells to recycle this raw material into cell-protective longevity proteins.

Temperature °C
20
Diet
OP50
Lifespan (days)
14.9
Lifespan comparisons
Triple mutant bec-1(RNAi);eat-2(ad1116);rrf-3(pk1426) has a lifespan of 14.9 days, while double mutant eat-2(ad1116);rrf-3(pk1426) has a lifespan of 19.3 days.
Type of interaction
See methods
Contains dependence
Citation
View abstract
Hansen M et al., 2008, A role for autophagy in the extension of lifespan by dietary restriction in C. elegans. PLoS Genet. 4(2):e24 18282106 Click here to select all mutants from this PubMed ID in the graph
Abstract
In many organisms, dietary restriction appears to extend lifespan, at least in part, by down-regulating the nutrient-sensor TOR (Target Of Rapamycin). TOR inhibition elicits autophagy, the large-scale recycling of cytoplasmic macromolecules and organelles. In this study, we asked whether autophagy might contribute to the lifespan extension induced by dietary restriction in C. elegans. We find that dietary restriction and TOR inhibition produce an autophagic phenotype and that inhibiting genes required for autophagy prevents dietary restriction and TOR inhibition from extending lifespan. The longevity response to dietary restriction in C. elegans requires the PHA-4 transcription factor. We find that the autophagic response to dietary restriction also requires PHA-4 activity, indicating that autophagy is a transcriptionally regulated response to food limitation. In spite of the rejuvenating effect that autophagy is predicted to have on cells, our findings suggest that autophagy is not sufficient to extend lifespan. Long-lived daf-2 insulin/IGF-1 receptor mutants require both autophagy and the transcription factor DAF-16/FOXO for their longevity, but we find that autophagy takes place in the absence of DAF-16. Perhaps autophagy is not sufficient for lifespan extension because although it provides raw material for new macromolecular synthesis, DAF-16/FOXO must program the cells to recycle this raw material into cell-protective longevity proteins.

Search genes: bec-1 eat-2 rrf-3 bec-1;eat-2;rrf-3

Entrez ID
Symbol
GenAge
Wormbase ID

177345
bec-1
View on GenAge (bec-1)
WBGene00000247

Beclin homolog

Locus: CELE_T19E7.3

Wormbase description: bec-1 encodes a coiled-coil protein orthologous to the yeast and mammalian autophagy proteins Atg6/Vps30/Beclin1; by homology, BEC-1 may be part of a Class III phosphatidylinositol 3-kinase complex that plays a role in localizing autophagy proteins to preautophagosomal structures and overexpression of C. elegans bec-1 in S. cerevisiae APG6/VPS30 mutants can rescue associated autophagy defects; bec-1 is also required for regulation of endocytic retrograde transport; in C. elegans, bec-1 activity is required for normal dauer morphogenesis and survival of dauer larvae, as well as for adult life span extension of daf-2(e1370) mutants at 15 degrees; in addition, bec-1(RNAi) indicates a role for bec-1 in normal growth rates, movement, and vulval morphogenesis; a bec-1::GFP reporter fusion is expressed in the hypodermis, intestine, nervous system, pharynx, and reproductive organs, all tissues that are remodeled during dauer larval development.

Entrez ID
Symbol
GenAge
Wormbase ID

175072
eat-2
View on GenAge (eat-2)
WBGene00001133

Neuronal acetylcholine receptor subunit eat-2

Locus: CELE_Y48B6A.4

Wormbase description: eat-2 encodes a ligand-gated ion channel subunit most closely related to the non-alpha-subunits of nicotinic acetylcholine receptors (nAChR); EAT-2 functions postsynaptically in pharyngeal muscle to regulate the rate of pharyngeal pumping; eat-2 is also required for normal life span and defecation; a functional EAT-2::GFP fusion protein localizes to two small dots near the junction of pharyngeal muscles pm4 and pm5, which is the site of the posterior-most MC motor neuron processes and the MC synapse; eat-2 genetically interacts with eat-18, which encodes a predicted novel transmembrane protein expressed in pharyngeal muscle and required for proper function of pharyngeal nicotonic receptors.

Entrez ID
Symbol
GenAge
Wormbase ID

174315
rrf-3
View on GenAge (rrf-3)
WBGene00004510

RNA-dependent RNA polymerase Family

Locus: CELE_F10B5.7

Wormbase description: rrf-3 encodes an RNA-directed RNA polymerase (RdRP) homolog that inhibits somatic RNAi, and thus promotes activity of repeated genes (e.g., multicopy transgenic arrays); the effect of RRF-3 on RNAi is opposite to that of RRF-1 (which stimulates somatic RNAi), which might arise from competition by RRF-3 with RRF-1 or EGO-1 in RNAi formation; rrf-3(allele) or rrf-3(allele2) mutants are hypersensitive to somatic RNAi, and conversely suppress the activity of an integrated rol6 (su1006) transgene.

Orthologs of bec-1;eat-2;rrf-3 in SynergyAge

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Species	Gene

Not in SynergyAge
Species	Gene

Orthologs of bec-1 in SynergyAge

Show in SynergyAge
Species	Gene

Not in SynergyAge
Species	Gene
Drosophila melanogaster	Atg6
Mus musculus	Becn1

Orthologs of eat-2 in SynergyAge

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Species	Gene

Orthologs of rrf-3 in SynergyAge

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Species	Gene