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You are what you eat: New insight into autophagy

Somewhere between cannibalism and recycling, the process known as autophagy plays a key role in regulating cell growth, metabolism and survival. Autophagy, literally gaining nutrition by consumption of one's own tissues, is a normal response to starvation in which portions of a cell are sequestered and digested so that the breakdown products can be used as a nutrient source. Now, adding to information about autophagy in single-celled organisms, two research papers published in the August issue of Developmental Cell shed new light on the molecular mechanisms of autophagy in the fruit fly, Drosophila.

The control of autophagy is regulated through multiple signaling pathways by nutritional, hormonal and developmental cues. The well-known regulators of nutrient signaling and cell growth, phosphoinositide 3-kinase (PI3K) and a downstream molecule called TOR, have been implicated in suppression of autophagy in mammalian cells. However, the mechanisms that link these effectors to autophagy in multicellular animals are poorly understood.

Researchers led by Dr. Harald Stenmark from The Norwegian Radium Hospital in Oslo examined autophagy in the Drosophila fat body using a microscope-based visualization technique. The Drosophila fat body stores nutrients in much the same way that the liver and fat tissue do in mammals. Starvation and inhibition of PI3K or TOR induced autophagy in the Drosophila fat body. "While the molecular machinery of autophagy is largely conserved from yeast to mammals, the control of autophagy in multicellular animals is necessarily more complex than in yeast, as it is likely to be involved in functions other than the starvation response," writes Dr. Stenmark. Stenmark's group went on to show that that ecdysone, an insect hormone regulating development, has the ability to promote programmed autophagy via downregulation of PI3K signaling.

A second study led by Dr. Thomas P. Neufeld from th
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Contact: Heidi Hardman
hhardman@cell.com
617-397-2879
Cell Press
9-Aug-2004


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