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Originally published In Press as doi:10.1074/jbc.M202737200 on June 21, 2002

J. Biol. Chem., Vol. 277, Issue 35, 31577-31584, August 30, 2002
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Xenopus Ribosomal RNA Gene Intergenic Spacer Elements Conferring Transcriptional Enhancement and Nucleolar Dominance-like Competition in Oocytes*

Amy A. CaudyDagger and Craig S. Pikaard§

From the Department of Biology, Washington University, St. Louis, Missouri 63130

Repeated within the intergenic spacers that separate adjacent ribosomal RNA (rRNA) genes in Xenopus laevis are several distinct sequence elements. These include transcription terminators, "region 0" repeats, "region 1" repeats, duplicated spacer promoters, and 42-bp enhancer elements that are embedded within 60 or 81-bp repeats. All have been reported to stimulate RNA polymerase I transcription from an adjacent gene promoter. A greater number of 42-bp enhancers/gene have been suggested to explain the preferential transcription of X. laevis rRNA genes in X. laevis x Xenopus borealis hybrids, an epigenetic phenomenon known as nucleolar dominance. However, the possible contribution of regions 0/1 and/or spacer promoters to the preferential transcription of X. laevis (over X. borealis) rRNA genes has never been tested directly. In this study, we systematically tested the various intergenic spacer elements for their contributions to promoter strength and nucleolar dominance-like competition in oocytes. In disagreement with a previous report, region 0 and region 1 repeats do not have significant enhancer activity, nor do they play a discernible role in X. laevis-X. borealis rRNA gene competition. Minigenes containing X. laevis spacer sequences are only dominant over minigenes having complete X. borealis spacers if a spacer promoter is located upstream of the 42-bp enhancers; X. laevis enhancers alone are not sufficient. These results provide additional evidence that spacer promoters together with adjacent enhancers form a functional activating unit in Xenopus oocytes.

* This work was supported by National Institutes of Grants R01-GM50910 and R01-GM60380 (to C. S. P.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger Supported by an Arthur Holly Compton Scholarship from Washington University, a Barry M. Goldwater Scholarship, and a Washington University/Howard Hughes Medical Institute Summer Undergraduate Research Fellowship funded by an Undergraduate Biological Sciences Education Program. Present address: Watson School of Biological Sciences, Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724.

§ To whom correspondence should be addressed: Dept. of Biology, Washington University, Campus Box 1137, 1 Brookings Dr., St. Louis, MO 63130. Tel.: 314-935-7569; Fax: 314-935-4432; E-mail: pikaard@biology.wustl.edu.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.


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