let-363;pep-2

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Genetic mutants with let-363, pep-2 alterations

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

Temperature °C
20
Lifespan (days)
22.2
Lifespan change (compared to wild type)
63.24%
Phenotype
All aspects of the let-363(RNAi_weak) phenotype were strongly enhanced in a pep-2(lg601) background
Lifespan comparisons
Double mutant let-363(RNAi);pep-2(lg601) has a lifespan of 22.2 days, while single mutant let-363(RNAi) has a lifespan of 18.3 days, single mutant pep-2(lg601) has a lifespan of 14.2 days and wild type has a lifespan of 13.6 days.
Type of interaction
See methods
Synergistic (positive)
Citation
View abstract
Meissner B et al., 2004, Deletion of the intestinal peptide transporter affects insulin and TOR signaling in Caenorhabditis elegans. J Biol Chem. 279(35):36739-45 15155758 Click here to select all mutants from this PubMed ID in the graph
Abstract
The mammalian intestinal peptide transporter PEPT1 mediates the uptake of di- and tripeptides from the gut lumen into intestinal epithelial cells and acts in parallel with amino acid transporters. Here we address the importance of the PEPT1 orthologue PEP-2 for the assimilation of dietary protein and for overall protein nutrition in Caenorhabditis elegans. pep-2 is expressed specifically along the apical membrane of the intestinal cells, and in pep-2 deletion mutant animals, uptake of intact peptides from the gut lumen is abolished. The consequences are a severely retarded development, reduced progeny and body size, and increased stress tolerance. We show here that pep-2 cross-talks with both the C. elegans target of rapamycin (TOR) and the DAF-2/insulin-signaling pathways. The pep-2 mutant enhances the developmental and longevity phenotypes of daf-2, resulting, among other effects, in a pronounced increase in adult life span. Moreover, all aspects of a weak let-363/TOR RNA interference phenotype are intensified by pep-2 deletion, indicating that pep-2 function upstream of TOR-mediated nutrient sensing. Our findings provide evidence for a predominant role of the intestinal peptide transporter for the delivery of bulk quantities of amino acids for growth and development, which consequently affects signaling pathways that regulate metabolism and aging.

Temperature °C
25
Lifespan (days)
15.8
Lifespan change (compared to wild type)
43.64%
Phenotype
The strong let-363(RNAi) phenotype cannot be enhanced further in a pep-2(lg601) mutant background.
Lifespan comparisons
Double mutant let-363(RNAi);pep-2(lg601) has a lifespan of 15.8 days, while single mutant let-363(RNAi) has a lifespan of 15.4 days, single mutant pep-2(lg601) has a lifespan of 9 days and wild type has a lifespan of 11 days.
Type of interaction
See methods
Opposite lifespan effects of single mutants
Citation
View abstract
Meissner B et al., 2004, Deletion of the intestinal peptide transporter affects insulin and TOR signaling in Caenorhabditis elegans. J Biol Chem. 279(35):36739-45 15155758 Click here to select all mutants from this PubMed ID in the graph
Abstract
The mammalian intestinal peptide transporter PEPT1 mediates the uptake of di- and tripeptides from the gut lumen into intestinal epithelial cells and acts in parallel with amino acid transporters. Here we address the importance of the PEPT1 orthologue PEP-2 for the assimilation of dietary protein and for overall protein nutrition in Caenorhabditis elegans. pep-2 is expressed specifically along the apical membrane of the intestinal cells, and in pep-2 deletion mutant animals, uptake of intact peptides from the gut lumen is abolished. The consequences are a severely retarded development, reduced progeny and body size, and increased stress tolerance. We show here that pep-2 cross-talks with both the C. elegans target of rapamycin (TOR) and the DAF-2/insulin-signaling pathways. The pep-2 mutant enhances the developmental and longevity phenotypes of daf-2, resulting, among other effects, in a pronounced increase in adult life span. Moreover, all aspects of a weak let-363/TOR RNA interference phenotype are intensified by pep-2 deletion, indicating that pep-2 function upstream of TOR-mediated nutrient sensing. Our findings provide evidence for a predominant role of the intestinal peptide transporter for the delivery of bulk quantities of amino acids for growth and development, which consequently affects signaling pathways that regulate metabolism and aging.

Search genes: let-363 pep-2

Entrez ID
Symbol
GenAge
Wormbase ID

172167
let-363
View on GenAge (let-363)
WBGene00002583

Target of rapamycin homolog

Locus: CELE_B0261.2

Wormbase description: none available

Symbol
GenAge

pep-2
View on GenAge (pep-2)

No gene information for pep-2

Orthologs of let-363;pep-2 in SynergyAge

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Species	Gene

Not in SynergyAge
Species	Gene

Orthologs of let-363 in SynergyAge

Show in SynergyAge
Species	Gene

Not in SynergyAge
Species	Gene
Drosophila melanogaster	Tor
Mus musculus	Mtor

Orthologs of pep-2 in SynergyAge

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Species	Gene