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Ternary complex factor-serum response factor complex-regulated gene activity is required for cellular proliferation

Elaine R Vickers1, Aneta Kasza, Isil Aksan Kurnaz

  • 1Faculty of Life Sciences, University of Manchester, Michael Smith Building, Oxford Rd., Manchester M13 9PT, United Kingdom.

Molecular and Cellular Biology
|November 16, 2004
PubMed

Insights

Inhibiting ternary complex factors (TCFs) blocks cell proliferation and triggers apoptosis by downregulating immediate-early genes. The antiapoptotic gene Mcl-1 is a key target, highlighting TCF-SRF

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Gene Regulation

Background:

  • Ternary complex factors (TCFs) are ETS-domain transcription factors activated by mitogen-activated protein kinases (MAPKs).
  • TCFs form a ternary complex with serum response factor (SRF) to activate serum response elements (SREs) in target gene promoters.
  • This complex is implicated in cell cycle entry and proliferation driven by mitogenic signaling.

Purpose of the Study:

  • To investigate the downstream gene regulatory and phenotypic effects of inhibiting TCF activity.
  • To elucidate the role of TCF-SRF complex in cell proliferation and apoptosis.

Main Methods:

  • Expression of a dominant-negative repressive form of TCF, Elk-1, to inhibit ternary complex activity.
  • Analysis of immediate-early gene expression.
  • Assessment of cell growth arrest and apoptosis.
  • Use of mutant Elk-1 alleles to confirm SRF-dependent mechanisms.

Main Results:

  • Inhibition of TCF activity led to downregulation of several immediate-early genes.
  • Blocking TCF-mediated gene expression resulted in growth arrest and triggered apoptosis.
  • SRF-dependent mechanisms mediated these effects.
  • The antiapoptotic gene Mcl-1 was identified as a key target of the TCF-SRF complex.

Conclusions:

  • TCF-SRF-regulated gene activity is crucial for regulating cell proliferation.
  • The TCF-SRF complex plays a role in protecting cells from apoptotic cell death.
  • Mcl-1 is a key downstream target mediating these effects.

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