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Related Experiment Videos

Comparative genomics on mammalian Fgf6-Fgf23 locus.

Yuriko Katoh1, Masaru Katoh

  • 1M&M Medical BioInformatics, Hongo 113-0033, Japan.

International Journal of Molecular Medicine
|July 14, 2005
PubMed
Summary

Comparative genomics reveals conserved regulatory elements in the FGF6-FGF23 gene cluster between humans and rodents. This finding aids in understanding the genetic basis of diseases like tumor-induced osteomalacia.

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Area of Science:

  • Genomics
  • Comparative Genomics
  • Molecular Biology

Background:

  • The FGF23 gene is implicated in hypophosphatemic disorders such as tumor-induced osteomalacia (TIO) and autosomal dominant hypophosphatemic rickets (ADHR).
  • Human chromosome 12p13.32 (CCND2-C12orf5-FGF23-FGF6 locus) and 11q13.3 (CCND1-ORAOV1-FGF19-FGF4 locus) represent paralogous regions in the human genome.

Purpose of the Study:

  • To conduct comparative genomic analyses of the human FGF6-FGF23 gene cluster and its rodent counterparts.
  • To identify conserved regulatory elements and understand the evolutionary conservation of these gene clusters.

Main Methods:

  • Bioinformatic determination of rat Fgf6 and Fgf23 complete coding sequences.
  • Identification and comparison of the FGF6-FGF23 gene clusters in human and rat genomes.
  • Analysis of intergenic conserved regions (IGCRs) and transcription factor binding sites in promoter regions.

Main Results:

  • Rat Fgf6 and Fgf23 genes were identified and found to be clustered in a tail-to-head manner, similar to their human orthologs.
  • A high nucleotide identity (77.6%) was observed between the human and rat FGF6-FGF23 intergenic conserved regions.
  • Conserved transcription factor binding sites (CP2, E47, CREB, PAX4 for FGF6; GATA, E47 for FGF23) were identified across species in the promoter regions.

Conclusions:

  • The study provides the first comparative genomics analysis of the human and rodent FGF6-FGF23 gene clusters.
  • Conserved regulatory elements suggest shared functional mechanisms and evolutionary history.
  • Dendritic cells are proposed as potential sources of FGF23 secretion in TIO patients, based on mouse Fgf23 mRNA expression patterns.

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