In Drosophila, the fat body undergoes a massive burst of autophagy at the end of larval development in preparation for the pupal transition. To identify genes involved in this process, we carried out a microarray analysis. We found that mRNA levels of the homologs of Atg8, the coat protein of early autophagic structures, and lysosomal hydrolases were upregulated, consistent with previous results. Genes encoding mitochondrial proteins and many chaperones were downregulated, including the inhibitor of eIF2alpha kinases and the peptidyl-prolyl cis-trans isomerase FK506-binding protein of 39 kDa (FKBP39). Genetic manipulation of FKBP39 expression had a significant effect on autophagy, potentially through modulation of the transcription factor Foxo. Accordingly, we found that Foxo mutants cannot properly undergo autophagy in response to starvation, and that overexpression of Foxo induces autophagy.

中文翻译：

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基因表达谱鉴定FKBP39为幼虫果蝇脂肪体内的自噬抑制剂。

在果蝇中，在幼体发育结束时，脂肪体会经历大量的自噬，为preparation的过渡做准备。为了鉴定参与该过程的基因，我们进行了微阵列分析。我们发现Atg8的同系物，早期自噬结构的外壳蛋白和溶酶体水解酶的mRNA水平被上调，与以前的结果一致。编码线粒体蛋白和许多伴侣的基因被下调，包括eIF2alpha激酶的抑制剂和39 kDa的肽基-脯氨酰顺反异构酶FK506结合蛋白（FKBP39）。FKBP39表达的遗传操纵可能通过调节转录因子Foxo对自噬产生重大影响。因此，我们发现Foxo突变体无法对饥饿做出适当的自噬，