scholarly journals Role of the ATPase/helicase maleless (MLE) in the assembly, targeting, spreading and function of the male-specific lethal (MSL) complex of Drosophila

2011 ◽  
Vol 4 (1) ◽  
pp. 6 ◽  
Author(s):  
Rosa Morra ◽  
Ruth Yokoyama ◽  
Huiping Ling ◽  
John C Lucchesi
Keyword(s):  
Male Specific Lethal ◽  
Msl Complex ◽  
And Function ◽  
Male Specific

Drosophila Male-Specific Lethal 2 Protein Controls Sex-Specific Expression of the roX Genes

Genetics ◽  
2004 ◽  
Vol 166 (4) ◽  
pp. 1825-1832 ◽  
Author(s):  
Barbara P Rattner ◽  
Victoria H Meller
Keyword(s):  
Gene Expression ◽  
Transcriptional Regulation ◽  
X Chromosome ◽  
Specific Expression ◽  
Linked Gene ◽  
Male And Female ◽  
Male Specific Lethal ◽  
Msl Complex ◽  
Male Specific ◽  
Rox Rna

Abstract The MSL complex of Drosophila upregulates transcription of the male X chromosome, equalizing male and female X-linked gene expression. Five male-specific lethal proteins and at least one of the two noncoding roX RNAs are essential for this process. The roX RNAs are required for the localization of MSL complexes to the X chromosome. Although the mechanisms directing targeting remain speculative, the ratio of MSL protein to roX RNA influences localization of the complex. We examine the transcriptional regulation of the roX genes and show that MSL2 controls male-specific roX expression in the absence of any other MSL protein. We propose that this mechanism maintains a stable MSL/roX ratio that is favorable for localization of the complex to the X chromosome.

scholarly journals Rapid Evolution of Autosomal Binding Sites of the Dosage Compensation Complex in Drosophila melanogaster and Its Association With Transcription Divergence

2021 ◽  
Vol 12 ◽  
Author(s):  
Aimei Dai ◽  
Yushuai Wang ◽  
Anthony Greenberg ◽  
Zhongqi Liufu ◽  
Tian Tang
Keyword(s):  
Drosophila Melanogaster ◽  
Dosage Compensation ◽  
Binding Sites ◽  
Protein Sequence ◽  
Rapid Evolution ◽  
Close Relative ◽  
Sequence Evolution ◽  
Male Specific Lethal ◽  
Msl Complex ◽  
Male Specific

How pleiotropy influences evolution of protein sequence remains unclear. The male-specific lethal (MSL) complex in Drosophila mediates dosage compensation by 2-fold upregulation of the X chromosome in males. Nevertheless, several MSL proteins also bind autosomes and likely perform functions not related to dosage compensation. Here, we study the evolution of MOF, MSL1, and MSL2 biding sites in Drosophila melanogaster and its close relative Drosophila simulans. We found pervasive expansion of the MSL binding sites in D. melanogaster, particularly on autosomes. The majority of these newly-bound regions are unlikely to function in dosage compensation and associated with an increase in expression divergence between D. melanogaster and D. simulans. While dosage-compensation related sites show clear signatures of adaptive evolution, these signatures are even more marked among autosomal regions. Our study points to an intriguing avenue of investigation of pleiotropy as a mechanism promoting rapid protein sequence evolution.

scholarly journals Painting of Fourth and the X-Linked 1.688 Satellite in D. melanogaster Is Involved in Chromosome-Wide Gene Regulation

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 323
Author(s):  
Samaneh Ekhteraei-Tousi ◽  
Jacob Lewerentz ◽  
Jan Larsson
Keyword(s):  
X Chromosome ◽  
Dosage Compensation ◽  
Rapid Evolution ◽  
Regulatory Mechanisms ◽  
Expression Of Genes ◽  
Male Specific Lethal ◽  
Msl Complex ◽  
Specific Regulation ◽  
Male Specific ◽  
Genomic Regions

Chromosome-specific regulatory mechanisms provide a model to understand the coordinated regulation of genes on entire chromosomes or on larger genomic regions. In fruit flies, two chromosome-wide systems have been characterized: The male-specific lethal (MSL) complex, which mediates dosage compensation and primarily acts on the male X-chromosome, and Painting of fourth (POF), which governs chromosome-specific regulation of genes located on the 4th chromosome. How targeting of one specific chromosome evolves is still not understood; but repeated sequences, in forms of satellites and transposable elements, are thought to facilitate the evolution of chromosome-specific targeting. The highly repetitive 1.688 satellite has been functionally connected to both these systems. Considering the rapid evolution and the necessarily constant adaptation of regulatory mechanisms, such as dosage compensation, we hypothesised that POF and/or 1.688 may still show traces of dosage-compensation functions. Here, we test this hypothesis by transcriptome analysis. We show that loss of Pof decreases not only chromosome 4 expression but also reduces the X-chromosome expression in males. The 1.688 repeat deletion, Zhr1 (Zygotic hybrid rescue), does not affect male dosage compensation detectably; however, Zhr1 in females causes a stimulatory effect on X-linked genes with a strong binding affinity to the MSL complex (genes close to high-affinity sites). Lack of pericentromeric 1.688 also affected 1.688 expression in trans and was linked to the differential expression of genes involved in eggshell formation. We discuss our results with reference to the connections between POF, the 1.688 satellite and dosage compensation, and the role of the 1.688 satellite in hybrid lethality.

scholarly journals Are we there yet? Initial targeting of the Male-Specific Lethal and Polycomb group chromatin complexes in Drosophila

Open Biology ◽  
2014 ◽  
Vol 4 (3) ◽  
pp. 140006 ◽  
Author(s):  
Kyle A. McElroy ◽  
Hyuckjoon Kang ◽  
Mitzi I. Kuroda
Keyword(s):  
Gene Expression ◽  
High Resolution ◽  
Biochemical Properties ◽  
Polycomb Group ◽  
Chromatin Binding ◽  
Male Specific Lethal ◽  
Msl Complex ◽  
Sites Of Action ◽  
Male Specific ◽  
Multicellular Organisms

Chromatin-binding proteins must navigate the complex nuclear milieu to find their sites of action, and a constellation of protein factors and other properties are likely to influence targeting specificity. Despite considerable progress, the precise rules by which binding specificity is achieved have remained elusive. Here, we consider early targeting events for two groups of chromatin-binding complexes in Drosophila : the Male-Specific Lethal (MSL) and the Polycomb group (PcG) complexes. These two serve as models for understanding targeting, because they have been extensively studied and play vital roles in Drosophila , and their targets have been documented at high resolution. Furthermore, the proteins and biochemical properties of both complexes are largely conserved in multicellular organisms, including humans. While the MSL complex increases gene expression and PcG members repress genes, the two groups share many similarities such as the ability to modify their chromatin environment to create active or repressive domains, respectively. With legacies of in-depth genetic, biochemical and now genomic approaches, the MSL and PcG complexes will continue to provide tractable systems for understanding the recruitment of multiprotein chromatin complexes to their target loci.

scholarly journals JIL-1 kinase, a member of the male-specific lethal (MSL) complex, is necessary for proper dosage compensation of eye pigmentation inDrosophila

genesis ◽  
2005 ◽  
Vol 43 (4) ◽  
pp. 213-215 ◽  
Author(s):  
Stephanie Lerach ◽  
Weiguo Zhang ◽  
Huai Deng ◽  
Xiaomin Bao ◽  
Jack Girton ◽  
...  
Keyword(s):  
Dosage Compensation ◽  
Male Specific Lethal ◽  
Eye Pigmentation ◽  
Msl Complex ◽  
Male Specific ◽  
Kinase A

scholarly journals Role of the Forkhead Transcription Factors Fd4 and Fd5 During Drosophila Leg Development

2021 ◽  
Vol 9 ◽  
Author(s):  
Mireya Ruiz-Losada ◽  
Cristian Pérez-Reyes ◽  
Carlos Estella
Keyword(s):  
Transcription Factors ◽  
Target Genes ◽  
Cell Fates ◽  
Forkhead Transcription Factors ◽  
Leg Development ◽  
Sex Comb ◽  
And Function ◽  
Male Specific ◽  
Redundant Role

Appendage development requires the coordinated function of signaling pathways and transcription factors to pattern the leg along the three main axes: the antero-posterior (AP), proximo-distal (PD), and dorso-ventral (DV). The Drosophila leg DV axis is organized by two morphogens, Decapentaplegic (Dpp), and Wingless (Wg), which direct dorsal and ventral cell fates, respectively. However, how these signals regulate the differential expression of its target genes is mostly unknown. In this work, we found that two members of the Drosophila forkhead family of transcription factors, Fd4 and Fd5 (also known as fd96Ca and fd96Cb), are identically expressed in the ventro-lateral domain of the leg imaginal disc in response to Dpp signaling. Here, we analyze the expression regulation and function of these genes during leg development. We have generated specific mutant alleles for each gene and a double fd4/fd5 mutant chromosome to study their function during development. We highlight the redundant role of the fd4/fd5 genes during the formation of the sex comb, a male specific structure that appears in the ventro-lateral domain of the prothoracic leg.

scholarly journals CLAMP directly interacts with MSL2 to facilitate Drosophila dosage compensation

2018 ◽  
Author(s):  
Evgeniya Tikhonova ◽  
Anna Fedotova ◽  
Artem Bonchuk ◽  
Vladic Mogila ◽  
Erica N. Larschan ◽  
...  
Keyword(s):  
X Chromosome ◽  
Dosage Compensation ◽  
Protein Complexes ◽  
Dna Binding Protein ◽  
Zinc Finger Domain ◽  
Dosage Compensation Complex ◽  
Dna Interactions ◽  
Male Specific Lethal ◽  
Msl Complex ◽  
Male Specific

AbstractThe binding of Drosophila male-specific lethal (MSL) dosage compensation complex exclusively to male X chromosome provides an excellent model system to understand mechanisms of selective recruitment of protein complexes to chromatin. Previous studies showed that the male-specific organizer of the complex, MSL2, and ubiquitous DNA-binding protein CLAMP are key players in the specificity of X chromosome binding. The CXC domain of MSL2 binds to genomic sites of MSL complex recruitment. Here we demonstrated that MSL2 directly interacts with the N-terminal zinc-finger domain of CLAMP. CLAMP-MSL2 and CXC-DNA interactions are cooperatively involved in recruitment of MSL complex to the X chromosome.

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