glp-1;lipl-4

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Genetic mutants with glp-1, lipl-4 alterations

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

Temperature °C
20
Diet
OP50; HT115E
Lifespan (days)
19.1
Lifespan comparisons
Double mutant glp-1(e2141);lipl-4(RNAi) has a lifespan of 19.1 days, while single mutant glp-1(e2141) has a lifespan of 23.0 days.
Citation
View abstract
Lapierre LR et al., 2011, Autophagy and lipid metabolism coordinately modulate life span in germline-less C. elegans. Curr Biol. 21(18):1507-14 21906946 Click here to select all mutants from this PubMed ID in the graph
Abstract
The cellular recycling process of autophagy is emerging as a key player in several longevity pathways in Caenorhabditis elegans. Here, we identify a role for autophagy in long-lived animals lacking a germline and show that autophagy and lipid metabolism work interdependently to modulate aging in this longevity model.

Temperature °C
20
Diet
OP50; HT115E
Lifespan (days)
15.3
Lifespan comparisons
Double mutant glp-1(e2141);lipl-4(RNAi) has a lifespan of 15.3 days, while single mutant glp-1(e2141) has a lifespan of 20.9 days.
Citation
View abstract
Lapierre LR et al., 2011, Autophagy and lipid metabolism coordinately modulate life span in germline-less C. elegans. Curr Biol. 21(18):1507-14 21906946 Click here to select all mutants from this PubMed ID in the graph
Abstract
The cellular recycling process of autophagy is emerging as a key player in several longevity pathways in Caenorhabditis elegans. Here, we identify a role for autophagy in long-lived animals lacking a germline and show that autophagy and lipid metabolism work interdependently to modulate aging in this longevity model.

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

Temperature °C
20
Diet
NGM
Lifespan (days)
20.66
Lifespan change (compared to wild type)
11.68%
Phenotype
GSC arrest caused by glp-1 loss of function resulted in extended life span; lipl-4 RNAi suppressed this increased longevity but did not reduce wild-type life span.
Lifespan comparisons
Double mutant glp-1(e2141ts);lipl-4(RNAi) has a lifespan of 20.66 days, while single mutant lipl-4(RNAi) has a lifespan of 19.64 days, single mutant glp-1(e2141ts) has a lifespan of 27.21 days and wild type has a lifespan of 18.5 days.
Type of interaction
See methods
Dependent
Citation
View abstract
Wang MC et al., 2008, Fat metabolism links germline stem cells and longevity in C. elegans. Science. 322(5903):957-60 18988854 Click here to select all mutants from this PubMed ID in the graph
Abstract
Fat metabolism, reproduction, and aging are intertwined regulatory axes; however, the mechanism by which they are coupled remains poorly understood. We found that germline stem cells (GSCs) actively modulate lipid hydrolysis in Caenorhabditis elegans, which in turn regulates longevity. GSC arrest promotes systemic lipolysis via induction of a specific fat lipase. Subsequently, fat mobilization is promoted and life span is prolonged. Constitutive expression of this lipase in fat storage tissue generates lean and long-lived animals. This lipase is a key factor in the lipid hydrolysis and increased longevity that are induced by decreased insulin signaling. These results suggest a link between C. elegans fat metabolism and longevity.

Temperature °C
20
Diet
NGM
Lifespan (days)
21.93
Lifespan change (compared to wild type)
10.70%
Phenotype
GSC arrest caused by glp-1 loss of function resulted in extended life span; lipl-4 RNAi suppressed this increased longevity but did not reduce wild-type life span.
Lifespan comparisons
Double mutant glp-1(e2141ts);lipl-4(RNAi) has a lifespan of 21.93 days, while single mutant lipl-4(RNAi) has a lifespan of 19.01 days, single mutant glp-1(e2141ts) has a lifespan of 26.19 days and wild type has a lifespan of 19.81 days.
Type of interaction
See methods
Opposite lifespan effects of single mutants
Citation
View abstract
Wang MC et al., 2008, Fat metabolism links germline stem cells and longevity in C. elegans. Science. 322(5903):957-60 18988854 Click here to select all mutants from this PubMed ID in the graph
Abstract
Fat metabolism, reproduction, and aging are intertwined regulatory axes; however, the mechanism by which they are coupled remains poorly understood. We found that germline stem cells (GSCs) actively modulate lipid hydrolysis in Caenorhabditis elegans, which in turn regulates longevity. GSC arrest promotes systemic lipolysis via induction of a specific fat lipase. Subsequently, fat mobilization is promoted and life span is prolonged. Constitutive expression of this lipase in fat storage tissue generates lean and long-lived animals. This lipase is a key factor in the lipid hydrolysis and increased longevity that are induced by decreased insulin signaling. These results suggest a link between C. elegans fat metabolism and longevity.

Search genes: glp-1 lipl-4

Entrez ID
Symbol
GenAge
Wormbase ID

176286
glp-1
View on GenAge (glp-1)
WBGene00001609

Protein glp-1

Locus: CELE_F02A9.6

Wormbase description: glp-1 encodes an N-glycosylated transmembrane protein that, along with LIN-12, comprises one of two C. elegans members of the LIN-12/Notch family of receptors; from the N- to the C-terminus, GLP-1 is characterized by ten extracellular EGF-like repeats, three LIN-12/Notch repeats, a CC-linker, a transmembrane domain, a RAM domain, six intracellular ankyrin repeats, and a PEST sequence; in C. elegans, GLP-1 activity is required for cell fate specification in germline and somatic tissues; in the germline, GLP-1, acting as a receptor for the DSL family ligand LAG-2, is essential for mitotic proliferation of germ cells and maintenance of germline stem cells; in somatic tissues, maternally provided GLP-1, acting as a receptor for the DSL family ligand APX-1, is required for inductive interactions that specify the fates of certain embryonic blastomeres; GLP-1 is also required for some later embryonic cell fate decisions, and in these decisions its activity is functionally redundant with that of LIN-12; GLP-1 expression is regulated temporally and spatially via translational control, as GLP-1 mRNA, present ubiquitously in the germline and embryo, yields detectable protein solely in lateral, interior, and endomembranes of distal, mitotic germ cells, and then predominantly in the AB blastomere and its descendants in the early embryo; proper spatial translation of glp-1 mRNA in the embryo is dependent upon genes such as the par genes, that are required for normal anterior-posterior asymmetry in the early embryo; signaling through GLP-1 controls the activity of the downstream Notch pathway components LAG-3 and LAG-1, the latter being predicted to function as part of a transcriptional feedback mechanism that positively regulates GLP-1 expression; signaling through the DNA-binding protein LAG-1 is believed to involve a direct interaction between LAG-1 and the GLP-1 RAM and ankyrin domains

Entrez ID
Symbol
GenAge
Wormbase ID

179046
lipl-4
View on GenAge (lipl-4)
WBGene00019376

LIPase Like;Lipase

Locus: CELE_K04A8.5

Wormbase description: lipl-4 encodes a triglyceride lipase; by homology, LIPL-4 is predicted to function in lipid hydrolysis; genetic studies indicate that lipl-4 functions as part of an endocrine signaling pathway that coordinates reproductive status, fat metabolism, and longevity; in response to reduced insulin signaling or germline removal (glp-1 mutant animals), lipl-4 expression is induced in the intestine, in a DAF-16-dependent manner; overexpression of lipl-4 can extend lifespan, in a manner dependent upon autophagy genes, such as bec-1, vps-34, and lgg-1.

Orthologs of glp-1;lipl-4 in SynergyAge

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Species	Gene

Not in SynergyAge
Species	Gene

Orthologs of glp-1 in SynergyAge

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Species	Gene

Orthologs of lipl-4 in SynergyAge

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Species	Gene

Not in SynergyAge
Species	Gene
Mus musculus	Lipo2
Mus musculus	Lipn
Mus musculus	Lipo3
Mus musculus	Lipk
Mus musculus	Lipm
Mus musculus	Lipf
Mus musculus	Lipa