Targeting of MOF, a putative histone acetyl transferase, to the X chromosome of Drosophila melanogaster
Article first published online: 6 DEC 1998
Copyright © 1998 Wiley-Liss, Inc.
Volume 22, Issue 1, pages 56–64, 1998
How to Cite
Gu, W., Szauter, P. and Lucchesi, J. C. (1998), Targeting of MOF, a putative histone acetyl transferase, to the X chromosome of Drosophila melanogaster. Dev. Genet., 22: 56–64. doi: 10.1002/(SICI)1520-6408(1998)22:1<56::AID-DVG6>3.0.CO;2-6
- Issue published online: 6 DEC 1998
- Article first published online: 6 DEC 1998
- Manuscript Accepted: 20 OCT 1997
- Manuscript Received: 14 SEP 1997
- NIH. Grant Number: GM15961
- dosage compensation complex;
- histone acetyl transferase
Dosage compensation ensures that males with a single X chromosome have the same amount of most X-linked gene products as females with two X chromosomes. In Drosophila, this equalization is achieved by a twofold enhancement of the level of transcription of the X in males relative to each X chromosome in females. The products of at least five genes, maleless (mle), male-specific lethal 1, 2, and 3 (msl-1, msl-2, msl-3) and males absent on the first (mof), are necessary for dosage compensation. The proteins produced by these genes form a complex that is preferentially associated with numerous sites on the X chromosome in somatic cells of males but not of females. Binding of the dosage compensation complex to the X chromosome is correlated with a significant increase in the presence of a specific histone isoform, histone 4 acetylated at lysine 16, on this chromosome. Experimental results and sequence analysis suggest that the mof gene encodes an acetyl transferase that plays a direct role in the specific histone acetylation associated with dosage compensation. Recently, RNA transcripts encoded by at least two different genes have also been found associated with the X chromosome in males.
We have studied the role played by the various components of the complex in the targeting of MOF to the X chromosome. To this end, we have used indirect cytoimmunofluorescence to monitor the binding of these components in males carrying complete or partial loss-of-function mutations as well as in XX individuals in which formation of the dosage compensation complex has been induced by genetic means. Dev. Genet. 22:56–64, 1998. © 1998 Wiley-Liss, Inc.