Institute for Chemical Research (ICR), Kyoto University, Uji, Kyoto 611-0011, Japan.
Genes Cells. 2011 Aug;16(8):857-67. doi: 10.1111/j.1365-2443.2011.01532.x.
In response to amino acid starvation, autophagy mediates the lysosome-dependent turnover of cytosolic components via autophagosome formation. Despite advances in understanding the molecular basis of autophagy process, the regulatory mechanism remains unclear. Here, we show that repression of protein synthesis stabilizes the messenger RNAs of specific autophagy-related (ATG) genes, increasing their respective half-lives. Further analysis indicated that the stabilization process is attributable to the coding region of the mRNAs. The results suggest a novel mechanism of autophagy regulation by post-transcriptional mRNA stabilization, in which repression of protein synthesis plays a direct role to sustain the autophagy process.
作为对氨基酸饥饿的反应，自噬通过自噬体的形成介导细胞溶质成分的溶酶体依赖性周转。尽管在理解自噬过程的分子基础方面取得了进展，但其调控机制仍不清楚。在这里，我们表明蛋白质合成的抑制稳定了特定自噬相关（ATG）基因的信使RNA，增加了它们各自的半衰期。进一步分析表明，稳定过程归因于mRNA的编码区。这些结果提示了一种通过转录后mRNA稳定来调控自噬的新机制，其中蛋白质合成的抑制在维持自噬过程中起直接作用。
