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Jun proteins inhibit autophagy and induce cell death

Orli Yogev1, Eitan Shaulian

  • 1Department of Biochemistry and Molecular Biology, IMRIC, Hebrew University-Hadassah Medical School, Jerusalem, Israel.

Autophagy
|April 21, 2010
PubMed

Insights

Starvation triggers autophagy for survival, but nutrients inhibit it for proliferation. Immediate early genes JunB and c-Jun block autophagy, potentially causing apoptosis in starved cells.

Area of Science:

  • Cellular biology
  • Molecular mechanisms of cell survival and proliferation

Background:

  • Autophagy is a cellular survival mechanism during starvation.
  • Nutrient and serum supplementation typically inhibit autophagy and promote cell proliferation.
  • Immediate early genes like JunB and c-Jun are induced by growth factors.

Purpose of the Study:

  • To investigate the role of immediate early genes JunB and c-Jun in regulating autophagy.
  • To understand how these genes influence cell fate under starvation and nutrient-rich conditions.

Main Methods:

  • Analysis of gene expression patterns during starvation and nutrient supplementation.
  • Investigating the inhibitory effect of JunB and c-Jun on the autophagic process.
  • Assessing the impact of JunB deregulation on cell fate in starved cells.

Main Results:

  • JunB and c-Jun were identified as inhibitors of autophagy.
  • Serum and growth factor induction of JunB and c-Jun suppresses the autophagic response.
  • Dysregulation of JunB during starvation promotes apoptosis.

Conclusions:

  • Immediate early genes JunB and c-Jun play a critical role in suppressing autophagy.
  • Aberrant expression of JunB can shift cell fate from survival (via autophagy) to apoptosis during starvation, highlighting a novel regulatory pathway.

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