An order-to-disorder structural switch activates the FoxM1 transcription factor

Elife. 2019 May 28:8:e46131. doi: 10.7554/eLife.46131.

Abstract

Intrinsically disordered transcription factor transactivation domains (TADs) function through structural plasticity, adopting ordered conformations when bound to transcriptional co-regulators. Many transcription factors contain a negative regulatory domain (NRD) that suppresses recruitment of transcriptional machinery through autoregulation of the TAD. We report the solution structure of an autoinhibited NRD-TAD complex within FoxM1, a critical activator of mitotic gene expression. We observe that while both the FoxM1 NRD and TAD are primarily intrinsically disordered domains, they associate and adopt a structured conformation. We identify how Plk1 and Cdk kinases cooperate to phosphorylate FoxM1, which releases the TAD into a disordered conformation that then associates with the TAZ2 or KIX domains of the transcriptional co-activator CBP. Our results support a mechanism of FoxM1 regulation in which the TAD undergoes switching between disordered and different ordered structures.

Keywords: Cdk; Plk1; human; intrinsically disordered proteins; molecular biophysics; nuclear magnetic resonance; structural biology; transcription factors.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Cycle Proteins / metabolism
  • Enzyme Activation*
  • Forkhead Box Protein M1 / chemistry*
  • Forkhead Box Protein M1 / metabolism*
  • Peptide Fragments / metabolism
  • Phosphorylation
  • Polo-Like Kinase 1
  • Protein Binding
  • Protein Conformation
  • Protein Domains
  • Protein Processing, Post-Translational
  • Protein Serine-Threonine Kinases / metabolism
  • Proto-Oncogene Proteins / metabolism
  • Sialoglycoproteins / metabolism

Substances

  • Cell Cycle Proteins
  • FOXM1 protein, human
  • Forkhead Box Protein M1
  • Peptide Fragments
  • Proto-Oncogene Proteins
  • Sialoglycoproteins
  • bone sialoprotein (35-62), human
  • Protein Serine-Threonine Kinases