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- W2073481808 abstract "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 AutophagyT.A. Gomez, K.L. Banfield, D.M. Trogler and S.G. ClarkeDevelopmental Biol 2007; 303:493-500" @default.
- W2073481808 created "2016-06-24" @default.
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- W2073481808 date "2007-07-16" @default.
- W2073481808 modified "2023-10-11" @default.
- W2073481808 title "Autophagy and Insulin/TOR Signaling in<i>Caenorhabditis elegans pcm-1</i>Protein Repair Mutants" @default.
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- W2073481808 doi "https://doi.org/10.4161/auto.4143" @default.
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