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Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
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Combinatorial gene control is the synergistic action of several transcriptional factors to regulate the expression of a single gene. The absence of one or more of these factors may lead to a significant difference in the level of gene expression or repression.
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DNA selection by the master transcription factor PU.1.

J Ross Terrell1, Samuel J Taylor2, Amelia L Schneider1

  • 1Department of Chemistry, Georgia State University, Atlanta, GA 30303, USA.

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|June 23, 2023
PubMed
Summary

The transcription factor PU.1 (Spi-1) binds DNA with varying strengths, influenced by its core sequence and flanking regions. A key glutamine (Q226) residue dictates DNA binding specificity and explains disease-related mutations.

Keywords:
CD11BCP: Molecular biologyCSF1RDNA methylationDNA specificityETS transcription factorsPU.1SPI1epigenetic regulationnon-canonical bindingprotein-DNA interactions

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Area of Science:

  • Molecular Biology
  • Structural Biology
  • Genetics

Background:

  • The transcription factor PU.1 (Spi-1) is crucial for myeloid gene regulation.
  • PU.1 exhibits a wide range of DNA binding affinities, a property not fully understood.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying PU.1's variable DNA binding affinities.
  • To characterize the structural basis of PU.1-DNA interactions across its affinity range.

Main Methods:

  • Co-crystallography of 22 PU.1/DNA complexes at high resolution.
  • Analysis of direct and indirect DNA readout mechanisms.
  • Phylogenetic and structural data re-synthesis of the ETS family.

Main Results:

  • Affinity is determined by a purine-rich core (e.g., 5'-GGAA-3') and flanking sequences.
  • Direct readout via glutamine 226 (Q226) specifies purine preference and explains pathogenic mutations (Q226E).
  • Indirect readout involves sequence-dependent helical flexibility, influencing binding to canonical and non-canonical sites.

Conclusions:

  • Q226 is central to PU.1's DNA binding specificity and plasticity.
  • Structural insights explain disease mutations and DNA methylation effects.
  • A unified model for DNA selection by ETS family proteins is proposed, centered on Q226.