Conservation and de novo acquisition of dosage compensation on newly evolved sex chromosomes in Drosophila
- Artyom A. Alekseyenko1,2,6,
- Christopher E. Ellison3,6,
- Andrey A. Gorchakov1,2,4,6,
- Qi Zhou3,
- Vera B. Kaiser3,
- Nick Toda3,
- Zaak Walton3,
- Shouyong Peng1,
- Peter J. Park1,5,
- Doris Bachtrog3,7 and
- Mitzi I. Kuroda1,2,7
- 1Division of Genetics, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA;
- 2Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA;
- 3Department of Integrative Biology, University of California at Berkeley, Berkeley, California 94720, USA;
- 4Institute of Molecular and Cell Biology, Novosibirsk 630090, Russia;
- 5Center for Biomedical Informatics, Harvard Medical School, Boston, Massachusetts 02115, USA
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↵6 These authors contributed equally to this work.
Abstract
Dosage compensation has arisen in response to the evolution of distinct male (XY) and female (XX) karyotypes. In Drosophila melanogaster, the MSL complex increases male X transcription approximately twofold. X-specific targeting is thought to occur through sequence-dependent binding to chromatin entry sites (CESs), followed by spreading in cis to active genes. We tested this model by asking how newly evolving sex chromosome arms in Drosophila miranda acquired dosage compensation. We found evidence for the creation of new CESs, with the analogous sequence and spacing as in D. melanogaster, providing strong support for the spreading model in the establishment of dosage compensation.
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Footnotes
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↵7 Corresponding authors
E-mail mkuroda{at}genetics.med.harvard.edu
E-mail dbachtrog{at}berkeley.edu
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Supplemental material is available for this article.
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Article is online at http://www.genesdev.org/cgi/doi/10.1101/gad.215426.113.
- Received February 3, 2013.
- Accepted March 29, 2013.
- Copyright © 2013 by Cold Spring Harbor Laboratory Press
