Comparative promoter analysis and its application in analysis of PTH-regulated gene expression

J Mol Biol. 2003 Mar 7;326(5):1327-36. doi: 10.1016/s0022-2836(03)00053-6.

Abstract

Taking advantage of the "working draft" of the human genome and the MIT shotgun assembly of the mouse genome, we performed a comparative promoter analysis of human RefSeq mRNA (sequences from GenBank's RefSeq database). By combining this analysis with a transcription factor (TF) binding site analysis using a TRANSFAC position weight matrix (PWM) search, 86% of non-specific TF sites were removed. Using a set of genes that are regulated by parathyroid hormone (PTH), a statistical analysis was performed on the conserved TF binding sites among a set of eight human and mouse genes. From among the eight genes tested, we obtained a set of 31 TFs, suggesting possible roles for associated genes in PTH-mediated pathways. All three known PTH-responsive TFs (AP1, RUNX2, CREB) were correctly predicted by this analysis as well as two other potential TFs (VDR and CEBP Delta). Additionally, a model was made to describe the TF site characteristic module of PTH-regulated genes. This model was then used to search all human RefSeq gene promoters with established human-mouse ortholog relationships to identify other PTH-regulated genes. This comparative approach combined with statistical analysis proved to be sufficiently specific to decipher critical TFs involved in PTH-regulated pathways.

Publication types

  • Comparative Study

MeSH terms

  • Algorithms
  • Animals
  • Computational Biology / methods*
  • Consensus Sequence
  • DNA Footprinting
  • Databases, Factual
  • Gene Expression Regulation / drug effects*
  • Genome*
  • Humans
  • Mice
  • Models, Biological
  • Parathyroid Hormone / pharmacology*
  • Promoter Regions, Genetic*
  • Receptors, Parathyroid Hormone
  • Response Elements
  • Signal Transduction
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*
  • Transcription, Genetic

Substances

  • Parathyroid Hormone
  • Receptors, Parathyroid Hormone
  • Transcription Factors