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The Drosophila gene hid is a direct molecular target of Ras-dependent survival signaling

A Bergmann1, J Agapite, K McCall

  • 1Massachusetts Institute of Technology, Howard Hughes Medical Institute, Department of Biology, Cambridge 02139, USA.

Cell
|November 14, 1998
PubMed

Insights

Growth factors promote cell survival by activating the Ras pathway, which inhibits cell death. This study reveals Ras signaling directly inactivates the proapoptotic gene head involution defective (hid) in Drosophila.

Area of Science:

  • Cell biology
  • Molecular biology
  • Developmental biology

Background:

  • Animal cell survival depends on extracellular growth factors.
  • Growth factors often signal via the Ras pathway.
  • Mechanisms by which Ras signaling inhibits cell death are not fully understood.

Purpose of the Study:

  • To investigate how Ras signaling inhibits intrinsic cell death.
  • To identify the molecular targets of Ras signaling in cell death inhibition.

Main Methods:

  • Utilized transgenic Drosophila animals.
  • Employed cultured Drosophila cells.
  • Analyzed the role of MAPK phosphorylation sites in the head involution defective (hid) gene.

Main Results:

  • Ras pathway activation specifically inhibits the proapoptotic activity of the gene head involution defective (hid) in Drosophila.
  • MAPK phosphorylation sites in Hid are crucial for this inhibition.
  • Demonstrated a novel mechanism of growth factor signaling in cell death regulation.

Conclusions:

  • Ras signaling directly inactivates a key component of the intrinsic cell death machinery.
  • Provides insights into the function of Ras as an oncogene.
  • Highlights a novel regulatory mechanism in cell survival and death pathways.

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