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Cell Death Differ. 2007 Jun;14(6):1181-90. Epub 2007 Mar 16.

Gene expression profiling identifies FKBP39 as an inhibitor of autophagy in larval Drosophila fat body.

Author information

1
Department of General Zoology, Eötvös Loránd University, Budapest, Hungary. juhas001@umn.edu

Abstract

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.

PMID:
17363962
PMCID:
PMC2084463
DOI:
10.1038/sj.cdd.4402123
[Indexed for MEDLINE]
Free PMC Article

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