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Oct1 is required for mTOR-induced G1 cell cycle arrest via the control of p27(Kip1) expression

Mathieu Dalvai1, Karin Schubart, Arnaud Besson

  • 1Friedrich Miescher Institute for Biomedical Research, Maulbeerstrase, Basel, Switzerland. Mathieu.dalvai@ibcg.biotoul.fr

Cell Cycle (Georgetown, Tex.)
|October 12, 2010
PubMed

Insights

Oct1 is crucial for cellular stress response, mediating growth arrest by controlling p27Kip1 expression. Cells lacking Oct1 bypass cell cycle arrest, highlighting Oct1

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Oct1 is a transcription factor induced by DNA damage.
  • Cellular stress response involves cell cycle regulation.
  • The mTOR pathway regulates cell proliferation and is sensitive to nutrient availability.

Purpose of the Study:

  • To investigate the role of Oct1 in the cellular stress response.
  • To determine Oct1's involvement in mTOR-mediated proliferation control.
  • To elucidate Oct1's function in nutrient starvation-induced cell cycle arrest.

Main Methods:

  • Utilized Oct1-deficient mouse embryonic fibroblasts.
  • Studied cell proliferation under glucose and amino acid starvation.
  • Assessed mTOR pathway activity and rapamycin sensitivity.
  • Analyzed the expression of CDK inhibitor p27Kip1.

Main Results:

  • Oct1-deficient cells proliferated continuously, bypassing G1 arrest during starvation.
  • mTOR-mediated proliferation control was abolished in Oct1-null cells.
  • Oct1-null cells were insensitive to mTOR inhibition by rapamycin or nutrient deprivation.
  • Oct1 controls p27Kip1 transcription downstream of mTOR; Oct1-null cells failed to upregulate p27Kip1.

Conclusions:

  • Oct1 is a critical mediator of growth arrest induced by mTOR inhibition.
  • Oct1 regulates p27Kip1 expression, essential for G1 arrest during nutrient stress.
  • Oct1 plays a key role in the cellular response to nutrient availability and stress.

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