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Molecular and Cellular Biology, February 2008, p. 958-966, Vol. 28, No. 3
0270-7306/08/$08.00+0     doi:10.1128/MCB.00995-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

The MLE Subunit of the Drosophila MSL Complex Uses Its ATPase Activity for Dosage Compensation and Its Helicase Activity for Targeting ^,

Rosa Morra,¹ Edwin R. Smith,^2, Ruth Yokoyama,¹ and John C. Lucchesi^1,3*

Department of Biology,¹ Department of Cell Biology,² Program in Genetics and Molecular Biology, Emory University, Atlanta, Georgia 30322³

Received 5 June 2007/ Returned for modification 6 August 2007/ Accepted 5 November 2007

In Drosophila, dosage compensation—the equalization of most X-linked gene products between XY males and XX females—is mediated by the MSL complex that preferentially associates with numerous sites on the X chromosome in somatic cells of males, but not of females. The complex consists of a noncoding RNA and a core of five protein subunits that includes a histone acetyltransferase (MOF) and an ATP-dependent DEXH box RNA/DNA helicase (MLE). Both of these enzymatic activities are necessary for the spreading of the complex to its sites of action along the X chromosome. MLE is related to the ATPases present in complexes that remodel chromatin by altering the positioning or the architectural relationship between nucleosomes and DNA. In contrast to MLE, none of these enzymatic subunits has been shown to possess double-stranded nucleic acid-unwinding activity. We investigated the function of MLE in the process of dosage compensation by generating mutations that separate ATPase activity from duplex unwinding. We show that the ATPase activity is sufficient for MLE's role in transcriptional enhancement, while the helicase activity is necessary for the spreading of the complex along the X chromosome.

Published ahead of print on 26 November 2007.

Supplemental material for this article may be found at http://mcb.asm.org/.

Present address: Stowers Institute for Medical Research, Kansas City, MO 64110.