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DNA bending in the ternary nucleoprotein complex at the c-fos promoter

A D Sharrocks1, P Shore

  • 1Department of Biochemistry and Genetics, Medical School, University of Newcastle upon Tyne, UK.

Insights

Serum response factor (SRF) binding to the c-fos promoter induces DNA bending. Elk-1 recruitment and MAP kinase phosphorylation further modify this DNA flexibility and bending, impacting c-fos gene transcription.

Area of Science:

  • Molecular Biology
  • Gene Regulation
  • Protein-DNA Interactions

Background:

  • The c-fos proto-oncogene's transcriptional induction by serum growth factors involves a ternary complex at the serum response element (SRE).
  • This complex comprises Elk-1, serum response factor (SRF), and the SRE, with Elk-1 phosphorylation by MAP kinase correlating with c-fos induction.

Purpose of the Study:

  • To investigate protein-induced DNA bending during the formation and post-translational modification of the ternary complex at the c-fos SRE.
  • To understand how SRF and Elk-1 binding, along with Elk-1 phosphorylation, influence DNA structure at the c-fos promoter.

Main Methods:

  • Circular permutation analysis to assess DNA bending induced by SRF.
  • Phasing analysis to determine the directionality and nature of DNA bending.
  • Investigated DNA bending changes upon Elk-1 binding and Elk-1 phosphorylation by MAP kinase (p42/ERK2).

Main Results:

  • The minimal DNA-binding domain of SRF (MADS box) is sufficient to induce flexibility and a directional bend towards the minor groove at the SRE.
  • Isolated ETS domains of Elk-1 and SAP-1 did not induce DNA bending.
  • Ternary complex formation with Elk-1 altered SRE flexibility, and Elk-1 phosphorylation caused minor flexibility changes.
  • Elk-1 recruitment modulated the SRF-induced directional DNA bend at the SRE.

Conclusions:

  • SRF binding induces significant DNA bending at the c-fos SRE, which is further modulated by Elk-1 binding and phosphorylation.
  • These structural changes in DNA flexibility and bending likely play roles in regulating c-fos transcription initiation.

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