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Article Addendum

Autophagy and Insulin/TOR Signaling in Caenorhabditis elegans pcm-1 Protein Repair Mutants

Tara A. Gomez and Steven G. Clarke

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Biological responses due to nutrient deprivation in the nematode Caenorhabditis elegans, including L1 diapause and autophagy during dauer formation, can be mediated through the linked DAF-2/insulin/IGF receptor and target-of-rapamycin (TOR) kinase pathways. Here we discuss how altered insulin/TOR signaling may underlie the previously reported phenotypes of worms with a null mutation in the pcm-1 gene that results in reduced autophagy during dauer formation and decreased L1 arrest survival. PCM-1 encodes a protein repair methyltransferase and mutants of the encoding pcm-1 gene are incapable of converting spontaneously damaged l-isoaspartyl residues in cellular proteins to normal forms by this pathway. We speculate that PCM-1 may function either directly or indirectly as an inhibitor of insulin/TOR signaling, perhaps in a role to balance autophagy with alternative protein degradation pathways that may be more specific for recognizing age-damaged proteins.

Addendum to:
The L-Isoaspartyl-O-Methyltransferase in Caenorhabditis elegans Larval Longevity and Autophagy
T.A. Gomez, K.L. Banfield, D.M. Trogler and S.G. Clarke
Developmental Biol 2007; 303:493-500

Authors

Tara A. Gomez

University of California, Los Angeles

Steven G. Clarke

University of California, Los Angeles

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If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.