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Mol Cell Biol, July 1998, p. 3668-3680, Vol. 18, No. 7
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Role of Histone H1 as an Architectural Determinant of Chromatin Structure and as a Specific Repressor of Transcription on Xenopus Oocyte 5S rRNA Genes

Takashi Sera and Alan P. Wolffe*

Laboratory of Molecular Embryology, National Institute of Child Health and Human Development, Bethesda, Maryland 20892-5431

Received 20 January 1998/Returned for modification 23 March 1998/Accepted 9 April 1998

We explore the role of histone H1 as a DNA sequence-dependent architectural determinant of chromatin structure and of transcriptional activity in chromatin. The Xenopus laevis oocyte- and somatic-type 5S rRNA genes are differentially transcribed in embryonic chromosomes in vivo depending on the incorporation of somatic histone H1 into chromatin. We establish that this effect can be reconstructed at the level of a single nucleosome. H1 selectively represses oocyte-type 5S rRNA genes by directing the stable positioning of a nucleosome such that transcription factors cannot bind to the gene. This effect does not occur on the somatic-type genes. Histone H1 binds to the 5' end of the nucleosome core on the somatic 5S rRNA gene, leaving key regulatory elements in the promoter accessible, while histone H1 binds to the 3' end of the nucleosome core on the oocyte 5S rRNA genes, specifically blocking access to a key promoter element (the C box). TFIIIA can bind to the somatic 5S rRNA gene assembled into a nucleosome in the presence of H1. Because H1 binds with equivalent affinities to nucleosomes containing either gene, we establish that it is the sequence-selective assembly of a specific repressive chromatin structure on the oocyte 5S rRNA genes that accounts for differential transcriptional repression. Thus, general components of chromatin can determine the assembly of specific regulatory nucleoprotein complexes.


* Corresponding author. Mailing address: Laboratory of Molecular Embryology, National Institute of Child Health and Human Development, NIH, Bldg. 18T, Rm. 106, Bethesda, MD 20892-5431. Phone: (301) 402-2722. Fax: (301) 402-1323. E-mail: awlme{at}helix.nih.gov.


Mol Cell Biol, July 1998, p. 3668-3680, Vol. 18, No. 7
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.



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