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Role of the insulin/Tor signaling network in starvation-induced programmed cell death in Drosophila oogenesis

T L Pritchett1, K McCall

  • 1Department of Biology, Boston University, 5 Cummington Street, Boston, MA 02215, USA.

Cell Death and Differentiation
|January 14, 2012
PubMed

Insights

Amino-acid starvation triggers programmed cell death (PCD) in Drosophila ovaries. Insulin signaling disruption prevents PCD, while Tor signaling independently regulates starvation-induced PCD.

Area of Science:

  • Developmental Biology
  • Cellular Biology
  • Genetics

Background:

  • Amino-acid starvation induces programmed cell death (PCD) and inhibits proliferation in Drosophila ovaries.
  • Insulin signaling disruption affects oogenesis, but its role in starvation-induced PCD is unclear.

Purpose of the Study:

  • To investigate if the insulin-mediated phosphoinositide kinase-3 pathway regulates PCD during mid-oogenesis in Drosophila.
  • To determine if disrupting insulin signaling mimics starvation-induced PCD.

Main Methods:

  • Generated Drosophila mutants with disrupted insulin signaling components in the germline.
  • Analyzed egg chamber morphology, caspase and lysosome induction, and PCD response to starvation.
  • Examined target of rapamycin (Tor) mutants for comparison.

Main Results:

  • Insulin signaling mutants produced abnormal egg chambers with lost somatic cells and persistent germlines, lacking typical PCD markers.
  • These mutants were resistant to starvation-induced PCD, indicating a necessary role for insulin signaling in the starvation response.
  • Target of rapamycin (Tor) mutants exhibited phenotypes mimicking wild-type starvation-induced PCD, suggesting insulin-independent regulation.

Conclusions:

  • Complete inhibition of insulin signaling is insufficient to induce starvation-like PCD in mid-oogenesis.
  • Starvation-induced PCD is regulated by Tor signaling, which converges with the canonical insulin signaling pathway.

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