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Epigenetic spreading of the Drosophila dosage compensation complex from roX RNA genes into flanking chromatin

Academic Article
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Overview

authors

  • Kelley, R. L.
  • Meller, V. H.
  • Gordadze, P. R.
  • Roman, G.
  • Davis, Ronald
  • Kuroda, M. I.

publication date

  • August 1999

journal

  • Cell  Journal

abstract

  • The multisubunit MSL dosage compensation complex binds to hundreds of sites along the Drosophila single male X chromosome, mediating its hypertranscription. The male X chromosome is also coated with noncoding roX RNAs. When either msl3, mle, or mof is mutant, a partial MSL complex is bound at only approximately 35 unusual sites distributed along the X. We show that two of these sites are the roX1 and roX2 genes and postulate that one of their functions is to provide entry sites for the MSL complex to recognize the X chromosome. The roX1 gene provides a nucleation site for extensive spreading of the MSL complex into flanking chromatin even when moved to an autosome. The spreading can occur in cis or in trans between paired homologs. We present a model for how the dosage compensation complex recognizes X chromatin.

subject areas

  • Animals
  • Chromatin
  • DNA
  • DNA-Binding Proteins
  • Dosage Compensation, Genetic
  • Drosophila
  • Drosophila Proteins
  • Drosophila melanogaster
  • Evolution, Molecular
  • Gene Expression Regulation
  • Genes, Insect
  • Insect Proteins
  • Male
  • Models, Genetic
  • Nuclear Proteins
  • Protein Binding
  • RNA
  • RNA-Binding Proteins
  • Species Specificity
  • Transcription Factors
  • Transcription, Genetic
  • Transgenes
  • X Chromosome
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Identity

International Standard Serial Number (ISSN)

  • 0092-8674

Digital Object Identifier (DOI)

  • 10.1016/s0092-8674(00)81979-0

PubMed ID

  • 10481915
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Additional Document Info

start page

  • 513

end page

  • 522

volume

  • 98

issue

  • 4

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