%0 Journal Article
%T Role of the ATPase/helicase maleless (MLE) in the assembly, targeting, spreading and function of the male-specific lethal (MSL) complex of Drosophila
%A Rosa Morra
%A Ruth Yokoyama
%A Huiping Ling
%A John C Lucchesi
%J Epigenetics & Chromatin
%D 2011
%I BioMed Central
%R 10.1186/1756-8935-4-6
%X The presence of the RB2 RNA-binding domain is necessary for the association of the MSL3 protein with the other complex subunits. In its absence, the activity of the MOF subunit was compromised, and the complex failed to acetylate histone H4 at lysine 16. Deletion of the RB1 RNA-binding domain resulted in complexes that maintained substantial acetylation activity but failed to spread beyond the high-affinity sites. Flies bearing this mutation exhibited low levels of roX RNAs, indicating that these RNAs failed to associate with the proteins of the complex and were degraded, or that MLE contributes to their synthesis. Deletion of the glycine-rich C-terminal region, which contains a nuclear localization sequence, caused a substantial level of retention of the other MSL proteins in the cytoplasm. These data suggest that the MSL proteins assemble into complexes or subcomplexes before entering the nucleus.This study provides insights into the role that MLE plays in the function of the MSL complex through its association with roX RNAs and the other MSL subunits, and suggests a hypothesis to explain the role of MLE in the synthesis of these RNAs.In Drosophila, dosage compensation (the equalization of many X-linked gene products between males with one X chromosome and females with two X chromosomes) is mediated by the male-specific lethal (MSL) complex, which consists of a core of five protein subunits (encoded by the genes male-specific lethal (msl) 1, 2 and 3, males absent on the first (mof), and maleless (mle)) and one of two non-coding RNAs (encoded by the genes RNA on the X (rox) 1 and 2). The complex preferentially associates with numerous sites on the X chromosome in somatic cells of males but not of females. It is responsible for an enhancement of the transcriptional rate of a large number of X-linked genes in males, thereby mediating a compensatory effect for the difference in dosage of these genes between males and females [1,2]. The presence of the MSL complex on t
%U http://www.epigeneticsandchromatin.com/content/4/1/6