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Molecular and Cellular Biology, April 2009, p. 2023-2031, Vol. 29, No. 8
0270-7306/09/$08.00+0 doi:10.1128/MCB.01448-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
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Department of Molecular, Cellular, and Developmental Biology, University of Michigan, Ann Arbor, Michigan 48109-1048
Received 15 September 2008/ Returned for modification 21 October 2008/ Accepted 23 January 2009
Dosage compensation equalizes X-linked gene products between the sexes. In Caenorhabditis elegans, the dosage compensation complex (DCC) binds both X chromosomes in XX animals and halves the transcription from each. The DCC is recruited to the X chromosomes by a number of loci, rex sites, and is thought to spread from these sites by an unknown mechanism to cover the rest of the chromosome. Here we describe a novel class of DCC-binding elements that we propose serve as "way stations" for DCC binding and spreading. Both rex sites and way stations comprise strong foci of DCC binding on the native X chromosome. However, rex sites maintain their ability to bind large amounts of DCC even on X duplications detached from the native X, while way stations do not. These results suggest that two distinct classes of DCC-binding elements facilitate recruitment and spreading of the DCC along the X chromosome.
Published ahead of print on 2 February 2009.
Supplemental material for this article may be found at http://mcb.asm.org/.
Present address: Stanford University Medical Center, 279 Campus Dr., Stanford, CA 94305-5323.
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