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

Tara A. Gomez and Steven G. Clarke

volume 3 | issue 4

July/August 2007
Pages: 357 - 359

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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

We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link: