Insulin and amino acid availability regulate atrogin-1 in avian QT6 cells
2007
Tesseraud, Sophie | Metayer-Coustard, Sonia | Boussaid, Sourour | Crochet, Sabine | Audouin, Estelle | Derouet, Michel | Seiliez, Iban
New evidence has demonstrated that the expression of major genes, termed atrogenes, controls the ubiquitin– roteasome proteolytic pathway. The present work aimed to study the impact of insulin and amino acids on the expression of one of these atrogenes, the E3 ubiquitin ligase Muscle Atrophy F box (MAFbx, also called atrogin-1), in quail muscle (QT6) fibroblasts. First, we characterized atrogin- 1 in QT6 cells and demonstrated the insulin sensitivity of these cells. Second, we showed that insulin reduced atrogin-1 mRNA via the phosphatidylinositol-30kinase (PI3K)/protein kinase B (PKB or AKT)/target of rapamycin (TOR) pathway. Atrogin-1 expression also depended on the availability of an individual amino acid, i.e., methionine. Moreover, the amino acid-induced reduction of atrogin-1 was inhibited by rapamycin, indicating the involvement of the TOR pathway in such regulation. In conclusion, expression of the ubiquitin ligase atrogin-1 is regulated by both insulin and amino acids through the TOR pathway
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