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Molecular and Cellular Biology, November 2007, p. 7865-7870, Vol. 27, No. 22
0270-7306/07/$08.00+0     doi:10.1128/MCB.00397-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

A Plasmid Model System Shows that Drosophila Dosage Compensation Depends on the Global Acetylation of Histone H4 at Lysine 16 and Is Not Affected by Depletion of Common Transcription Elongation Chromatin Marks{triangledown} ,{dagger}

Ruth Yokoyama,1 Antonio Pannuti,1,{ddagger} Huiping Ling,1 Edwin R. Smith,2,§ and John C. Lucchesi1*

Department of Biology,1 Department of Cell Biology, Emory University, Atlanta, Georgia 303222

Received 6 March 2007/ Returned for modification 10 April 2007/ Accepted 31 August 2007

Dosage compensation refers to the equalization of most X-linked gene products between males, which have one X chromosome and a single dose of X-linked genes, and females, which have two X's and two doses of such genes. We developed a plasmid-based model of dosage compensation that allows new experimental approaches for the study of this regulatory mechanism. In Drosophila melanogaster, an enhanced rate of transcription of the X chromosome in males is dependent upon the presence of histone H4 acetylated at lysine 16. This chromatin mark occurs throughout active transcriptional units, leading us to the conclusion that the enhanced level of transcription is achieved through an enhanced rate of RNA polymerase elongation. We used the plasmid model to demonstrate that enhancement in the level of transcription does not depend on other histone marks and factors that have been associated with the process of elongation, thereby highlighting the special role played by histone H4 acetylated at lysine 16 in this process.

* Corresponding author. Mailing address: Department of Biology, Emory University, 1510 Clifton Rd. NE, Atlanta, GA 30322. Phone: (404) 727-4943. Fax: (404) 727-2880. E-mail: lucchesi{at}biology.emory.edu

{triangledown} Published ahead of print on 17 September 2007.

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

{ddagger} Present address: Cancer Research Center of Hawaii, Honolulu, HI 96813.

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

Molecular and Cellular Biology, November 2007, p. 7865-7870, Vol. 27, No. 22
0270-7306/07/$08.00+0     doi:10.1128/MCB.00397-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Gelbart, M. E., Kuroda, M. I. (2009). Drosophila dosage compensation: a complex voyage to the X chromosome. Development 136: 1399-1410 [Abstract] [Full Text]  
  • Park, S.-W., Kuroda, M. I., Park, Y. (2008). Regulation of Histone H4 Lys16 Acetylation by Predicted Alternative Secondary Structures in roX Noncoding RNAs. Mol. Cell. Biol. 28: 4952-4962 [Abstract] [Full Text]  
  • Bell, O., Conrad, T., Kind, J., Wirbelauer, C., Akhtar, A., Schubeler, D. (2008). Transcription-Coupled Methylation of Histone H3 at Lysine 36 Regulates Dosage Compensation by Enhancing Recruitment of the MSL Complex in Drosophila melanogaster. Mol. Cell. Biol. 28: 3401-3409 [Abstract] [Full Text]  
  • Morra, R., Smith, E. R., Yokoyama, R., Lucchesi, J. C. (2008). The MLE Subunit of the Drosophila MSL Complex Uses Its ATPase Activity for Dosage Compensation and Its Helicase Activity for Targeting. Mol. Cell. Biol. 28: 958-966 [Abstract] [Full Text]  


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