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Gene Review:

let-363 - Protein LET-363

Caenorhabditis elegans

Long, X. et al., Casanova, J. et al., Meissner, B. et al., Jia, K. et al.

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High impact information on let-363

Several genes are normally required for activating tor and appear to define a system in which a gene product tethered to the extracellular vitelline membrane at each end of the egg provides a local source for an extracellular tor ligand [1].
We report that in C. elegans, mutations in the genes encoding CeTOR and raptor result in dauer-like larval arrest, implying that CeTOR regulates dauer diapause [2].
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 [3].
Inactivation of C. elegans p70S6K or TAP42 homologs does not reproduce CeTOR deficiency phenotypes, nor does inactivation of C. elegans TIP41, a putative negative regulator of CeTOR function, rescue CeTOR deficiency [4].

Biological context of let-363

We describe a C. elegans TOR homolog (CeTOR) and phenotypes associated with CeTOR deficiency [4].

References

The torso receptor localizes as well as transduces the spatial signal specifying terminal body pattern in Drosophila. Casanova, J., Struhl, G. Nature (1993) [Pubmed]
The TOR pathway interacts with the insulin signaling pathway to regulate C. elegans larval development, metabolism and life span. Jia, K., Chen, D., Riddle, D.L. Development (2004) [Pubmed]
Deletion of the intestinal peptide transporter affects insulin and TOR signaling in Caenorhabditis elegans. Meissner, B., Boll, M., Daniel, H., Baumeister, R. J. Biol. Chem. (2004) [Pubmed]
TOR deficiency in C. elegans causes developmental arrest and intestinal atrophy by inhibition of mRNA translation. Long, X., Spycher, C., Han, Z.S., Rose, A.M., Müller, F., Avruch, J. Curr. Biol. (2002) [Pubmed]

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