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Warts is required for PI3K-regulated growth arrest, autophagy, and autophagic cell death in Drosophila

Sudeshna Dutta1, Eric H Baehrecke

  • 1Molecular and Cell Biology Program, University of Maryland, College Park, Maryland 20742, USA.

Current Biology : CB
|September 27, 2008
PubMed
Abstract

Insights

The Warts (Wts) pathway is crucial for salivary gland cell death in Drosophila, regulating growth arrest and autophagy. PI3K signaling is key to Wts

Area of Science:

  • Developmental Biology
  • Cell Biology
  • Genetics

Background:

  • Cell growth arrest and autophagy are essential for autophagic cell death in Drosophila.
  • Growth-promoting pathways (Ras, Dp110, Akt) inhibit autophagy and cell death in Drosophila salivary glands.
  • The Warts (Wts) tumor suppressor regulates tissue growth, but its role in controlling cell growth arrest is unclear.

Purpose of the Study:

  • To investigate the role of the Warts (Wts) pathway in regulating salivary gland cell death, growth arrest, and autophagy in Drosophila.
  • To elucidate the mechanism by which Wts signaling controls cell growth and influences autophagic cell death.

Main Methods:

  • Genetic analysis of Warts (Wts) pathway mutants in Drosophila salivary glands.
  • Assessment of cell growth arrest, caspase activity, and autophagy.
  • Functional studies involving expression of autophagy regulators (Atg1) and Wts pathway components (Yki, Sd, bantam).
  • Analysis of phosphoinositide signaling and PI3K pathway components (chico, TOR).

Main Results:

  • Wts pathway genes are required for salivary gland degradation; wts mutants exhibit defects in cell growth arrest, caspase activity, and autophagy.
  • Expression of Atg1 rescues wts mutant salivary gland destruction, indicating a role in autophagy.
  • Wts regulates salivary gland cell death in a PI3K-dependent manner, with chico and TOR mutations suppressing wts defects.

Conclusions:

  • This study provides the first evidence that Warts (Wts) signaling influences autophagy.
  • Wts pathway components Yki, Sd, and bantam appear not to function in Drosophila salivary glands.
  • Wts regulates salivary gland cell death through a mechanism dependent on phosphoinositide 3-kinase (PI3K) signaling.

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