70
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Transcription factor hierarchy in Waardenburg syndrome: regulation of MITF expression by SOX10 and PAX3.

      Human genetics
      Animals, Base Sequence, Conserved Sequence, DNA-Binding Proteins, biosynthesis, genetics, Evolution, Molecular, Gene Deletion, Gene Expression Regulation, Genes, Dominant, Genotype, HeLa Cells, High Mobility Group Proteins, Humans, Mice, Mice, Inbred C3H, Mice, Inbred C57BL, Mice, Mutant Strains, Microphthalmia-Associated Transcription Factor, Molecular Sequence Data, Mutagenesis, Mutation, Paired Box Transcription Factors, Phenotype, Promoter Regions, Genetic, SOXE Transcription Factors, Sequence Homology, Nucleic Acid, Time Factors, Transcription Factors, Transfection, Waardenburg Syndrome

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Waardenburg syndrome (WS) is associated with neural crest-derived melanocyte deficiency caused by mutations in either one of three transcription factors: MITF, PAX3, and SOX10. However, the hierarchical relationship of these transcription factors is largely unknown. We show that SOX10 is capable of transactivating the MITF promoter 100-fold, and that this transactivation is further stimulated by PAX3. Promoter deletion and mutational analyses indicate that SOX10 can activate MITF expression through binding to a region that is evolutionarily conserved between the mouse and human MITF promoters. A SOX10 mutant that models C-terminal truncations in WS can reduce wild-type SOX10 induction of MITF, suggesting these mutations may act in a dominant-negative fashion. Our data support a model in which the hypopigmentation in WS, of which these factors have been implicated, results from a disruption in function of the central melanocyte transcription factor MITF.

          Related collections

          Author and article information

          Comments

          Comment on this article