Lifespan changes: From wild type to cul-6;glp-1
20
25.9
39.25%
Unlike the general proteasomal subunits, RNAi-knockdown of Cullins did not shorten the lifespan of glp-1(e2141ts) mutants or wild-type worms. In fact, some RNAi treatments further extended the glp-1-mutant lifespan. These findings suggest that reducing Cullin function does not generally shorten lifespan, but instead that Cullin complexes might selectively influence the longevity of particular mutants.
Double mutant cul-6(RNAi);glp-1(e2141ts) has a lifespan of 25.9 days, while single mutant glp-1(e2141ts) has a lifespan of 22.4 days, single mutant cul-6(RNAi) has a lifespan of 19.7 days and wild type has a lifespan of 18.6 days.
Synergistic (positive)
Ghazi A et al., 2007, Regulation of Caenorhabditis elegans lifespan by a proteasomal E3 ligase complex. Proc Natl Acad Sci U S A. 104(14):5947-52 17392428 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
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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