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Laser Microdissection Applied to Gene Expression Profiling of Subset of Cells from the Drosophila Wing Disc

Published on: May 1, 2010

Ras1 promotes cellular growth in the Drosophila wing

D A Prober1, B A Edgar

  • 1Molecular and Cellular Biology Program, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA.

Cell
|February 29, 2000
PubMed

Insights

Ras GTPase signaling controls cell proliferation by regulating cell growth and G1/S phase transitions. Activating Ras boosts growth and cell cycle progression, while inactivating Ras hinders growth and causes apoptosis in Drosophila.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Molecular Biology

Background:

  • Ras GTPase is a key regulator linking extracellular signals to cell proliferation.
  • Understanding Ras function in vivo is crucial for deciphering growth control mechanisms.

Purpose of the Study:

  • To investigate the in vivo role of Ras in regulating cell proliferation in Drosophila.
  • To elucidate the downstream effectors and cell cycle targets of Ras signaling.

Main Methods:

  • Ras activation and inactivation in specific cell clones within the developing Drosophila wing.
  • Analysis of cell size, growth rates, cell cycle progression (G1, G2/M), and apoptosis.
  • Assessment of key regulatory molecules including dMyc and cyclin E levels.

Main Results:

  • Ras inactivation led to reduced cell size, slower growth, G1 cell cycle arrest, and apoptosis via cell competition.
  • Ras activation increased cell size, growth rates, and promoted G1/S phase transitions.
  • Ras and its downstream effector dMyc upregulated cyclin E levels posttranscriptionally.
  • Ras-mediated growth enhancement did not disrupt G2/M progression or normal cell cycle exit.

Conclusions:

  • Ras primarily functions to promote cell growth, which is tightly coupled to G1/S phase progression through cyclin E.
  • Ras signaling is essential for maintaining cell growth and survival during development.
  • Ras-mediated growth regulation is distinct from its effects on later cell cycle phases and developmental cell cycle exit.

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