Uncovering a macrophage transcriptional program by integrating evidence from motif scanning and expression dynamics

PLoS Comput Biol. 2008 Mar 21;4(3):e1000021. doi: 10.1371/journal.pcbi.1000021.

Abstract

Macrophages are versatile immune cells that can detect a variety of pathogen-associated molecular patterns through their Toll-like receptors (TLRs). In response to microbial challenge, the TLR-stimulated macrophage undergoes an activation program controlled by a dynamically inducible transcriptional regulatory network. Mapping a complex mammalian transcriptional network poses significant challenges and requires the integration of multiple experimental data types. In this work, we inferred a transcriptional network underlying TLR-stimulated murine macrophage activation. Microarray-based expression profiling and transcription factor binding site motif scanning were used to infer a network of associations between transcription factor genes and clusters of co-expressed target genes. The time-lagged correlation was used to analyze temporal expression data in order to identify potential causal influences in the network. A novel statistical test was developed to assess the significance of the time-lagged correlation. Several associations in the resulting inferred network were validated using targeted ChIP-on-chip experiments. The network incorporates known regulators and gives insight into the transcriptional control of macrophage activation. Our analysis identified a novel regulator (TGIF1) that may have a role in macrophage activation.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Amino Acid Motifs
  • Animals
  • Computer Simulation
  • Gene Expression Regulation / physiology
  • Humans
  • Kinetics
  • Macrophage Activation / physiology*
  • Macrophages / physiology*
  • Models, Biological*
  • Signal Transduction / physiology*
  • Structure-Activity Relationship
  • Systems Integration
  • Toll-Like Receptors / metabolism*
  • Transcription Factors / physiology*
  • Transcriptional Activation / physiology*

Substances

  • Toll-Like Receptors
  • Transcription Factors