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An Ecdysone Receptor-based Singular Gene Switch for Deliberate Expression of Transgene with Robustness, Reversibility, and Negligible Leakiness
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ERK-ERF-EGR1, a novel switch underlying acquisition of a motile phenotype

Nir Ben-Chetrit1, Gabi Tarcic, Yosef Yarden

  • 1Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.

Cell Adhesion & Migration
|October 19, 2012
PubMed

Insights

Cell migration commitment involves early and late molecular switches. A novel ERK-ERF-EGR1 pathway in human mammary cells controls cell migration by regulating gene expression.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Signal Transduction

Background:

  • Cell cycle commitment is well-understood, but pathways driving cell migration are not.
  • Extracellular cues like epidermal growth factor (EGF) activate molecular switches for migration.
  • Early (transcription-independent) and late (transcription-dependent) switches contribute to cell motility.

Discussion:

  • This review focuses on early and late molecular switches governing cell migration.
  • A novel ERK-ERF-EGR1 switch in human mammary cells is highlighted.
  • The study contrasted pathways for EGF-induced migration and serum-stimulated growth.

Key Insights:

  • Epidermal growth factor (EGF) stimulates human mammary cell migration.
  • Serum factors stimulate human mammary cell growth.
  • A novel cascade involves the ERK mitogen-activated protein kinase (MAPK) pathway exporting the ERF repressor from the nucleus.

Outlook:

  • This export permits balanced stimulation of an EGR1-centered gene expression program.
  • Understanding these migration commitment pathways is crucial for various biological processes.
  • Further research into these transcription-dependent and independent mechanisms is warranted.

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