Long-range spreading of dosage compensation in Drosophila captures transcribed autosomal genes inserted on X
- Andrey A. Gorchakov1,2,3,
- Artyom A. Alekseyenko1,2,
- Peter Kharchenko4,5,
- Peter J. Park4,5 and
- Mitzi I. Kuroda1,2,6
- 1Division of Genetics, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA;
- 2Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA;
- 3Department of Molecular and Cellular Biology, Institute of Chemical Biology and Fundamental Medicine SB RAS, Novosibirsk 630090, Russia;
- 4Center for Biomedical Informatics, Harvard Medical School, Boston, Massachusetts 02115, USA;
- 5Informatics Program, Children's Hospital, Boston, Massachusetts 02115, USA
Abstract
Dosage compensation in Drosophila melanogaster males is achieved via targeting of male-specific lethal (MSL) complex to X-linked genes. This is proposed to involve sequence-specific recognition of the X at ∼150–300 chromatin entry sites, and subsequent spreading to active genes. Here we ask whether the spreading step requires transcription and is sequence-independent. We find that MSL complex binds, acetylates, and up-regulates autosomal genes inserted on X, but only if transcriptionally active. We conclude that a long-sought specific DNA sequence within X-linked genes is not obligatory for MSL binding. Instead, linkage and transcription play the pivotal roles in MSL targeting irrespective of gene origin and DNA sequence.
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Footnotes
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↵6 Corresponding author.
E-MAIL mkuroda{at}genetics.med.harvard.edu; FAX (617) 525-4522.
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Article is online at http://www.genesdev.org/cgi/doi/10.1101/gad.1840409.
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Supplemental material is available at http://www.genesdev.org.
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- Received July 7, 2009.
- Accepted August 20, 2009.
- Copyright © 2009 by Cold Spring Harbor Laboratory Press
