Hedgehog and Wingless signaling are not essential for autophagy-dependent cell death

Tianqi Xu1, Donna Denton1, Sharad Kumar1

  • 1Centre for Cancer Biology, University of South Australia & SA Pathology, GPO Box 2471, Adelaide, SA 5001, Australia.

Insights

Autophagy-dependent cell death in Drosophila midgut removal is not regulated by Hedgehog (Hh) or Wingless (Wg) signaling. However, Glycogen Synthase Kinase 3 (Sgg) may control cell size independently of these pathways.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Genetics

Background:

  • Autophagy-dependent cell death is a specific form of programmed cell death.
  • The Drosophila larval midgut's removal during metamorphosis is a key model for studying this process.
  • Previous work established that reduced growth signaling is crucial for autophagy induction and midgut degradation.

Purpose of the Study:

  • To investigate the roles of Hedgehog (Hh) and Wingless (Wg) signaling pathways in autophagy-dependent cell death during Drosophila midgut remodeling.
  • To understand the regulation of autophagy and cell death during the larval-pupal transition.

Main Methods:

  • Utilized Drosophila melanogaster as a genetic model system.
  • Investigated the involvement of Hh and Wg signaling pathways.
  • Examined the function of Glycogen Synthase Kinase 3 (Sgg).

Main Results:

  • Hedgehog (Hh) and Wingless (Wg) signaling pathways do not regulate autophagy-dependent cell death in the Drosophila midgut.
  • Sustained growth signaling via Ras and PI3K inhibits autophagy and midgut degradation.
  • Dpp signaling is important for the timing of midgut degradation.
  • Surprisingly, Shaggy (Sgg), a key component of Hh and Wg pathways, appears to regulate midgut cell size independently of Hh and Wg.

Conclusions:

  • Hh and Wg signaling are not essential regulators of autophagy-dependent cell death during Drosophila midgut regression.
  • Shaggy (Sgg) has a potential role in controlling cell size independent of its canonical Hh and Wg pathway functions.
  • Further research is needed to elucidate the precise mechanisms of Sgg in cell size regulation.

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