Lifespan changes: From wild type to glp-1;lgg-1
20
OP50; HT115E
19.6
9.50%
RNAi inhibition of bec-1significantly reduced the mean lifespan of glp-1(e2141) animals.
Double mutant glp-1(e2141);lgg-1(RNAi) has a lifespan of 19.6 days, while single mutant lgg-1(RNAi) has a lifespan of 18.0 days, single mutant glp-1(e2141) has a lifespan of 24.0 days and wild type has a lifespan of 17.9 days.
Dependent
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
20
OP50; HT115E
19.9
7.57%
RNAi inhibition of lgg-1significantly reduced the mean lifespan of glp-1(e2141) animals.
Double mutant glp-1(e2141);lgg-1(RNAi) has a lifespan of 19.9 days, while single mutant lgg-1(RNAi) has a lifespan of 20.2 days, single mutant glp-1(e2141) has a lifespan of 24.2 days and wild type has a lifespan of 18.5 days.
Antagonistic (positive)
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
20
OP50; HT115E
12.3
-35.94%
RNAi inhibition of lgg-1significantly reduced the mean lifespan of glp-1(e2141) animals.
Double mutant glp-1(e2141);lgg-1(RNAi) has a lifespan of 12.3 days, while single mutant lgg-1(RNAi) has a lifespan of 18.8 days, single mutant glp-1(e2141) has a lifespan of 20.3 days and wild type has a lifespan of 19.2 days.
Opposite lifespan effects of single mutants
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
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
Protein lgg-1
Locus: CELE_C32D5.9
Wormbase description: lgg-1 encodes the C. elegans ortholog of Saccharomyces cerevisiae Atg8p and mammalian MAP-LC3; by homology, LGG-1 is predicted to be required for the degradation of cellular components by autophagy; loss of lgg-1 function via RNAi indicates that, like several other C. elegans genes involved in autophagy, lgg-1 is essential for normal dauer morphogenesis and life-span extension; a GFP::LGG-1 reporter fusion protein is expression in several different stages of development in multiple tissues, including the nervous system, pharynx, intestine, hypodermis, somatic gonad and vulva; under normal growth conditions, GFP::LGG-1 shows a diffuse cytoplasmic localization, but during dauer formation and in long-lived animals, GFP::LGG-1 shows a marked increase in punctate staining in hypodermal seam cells that likely reflects an increase in the number of preautophagosomal and autophagosomal structures.
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SynergyAge database hosts high-quality, manually curated information about the synergistic and antagonistic lifespan effects of genetic interventions in model organisms, also allowing users to explore the longevity relationships between genes in a visual way.
If you would like to cite this database please use:
Bunu, G., Toren, D., Ion, C. et al. SynergyAge, a curated database for synergistic and antagonistic interactions of longevity-associated genes. Sci Data 7, 366 (2020). https://doi.org/10.1038/s41597-020-00710-z
Group webpage: www.aging-research.group