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MSL2 is required for upregulation of male X chromosome but not for expression of autosomal genes

ABSTRACT: Drosophila males double transcription of their single X chromosome to equalize X-linked gene expression with females, which carry two X chromosomes. Increased transcription requires the Male-Specific Lethal (MSL) complex. The MSL2 protein is essential component of the MSL complex. MSL2 is the only protein that is strictly limited to males. MSL2 together with MSL1 forms the core of the MSL complex. The global effect of msl2 mutation on gene expression was measured by microarray analysis. We found that expression of the X chromosome was decreased in msl21 male larvae, supporting the involvement of MSL2 in the up-regulation of X-linked genes. However, there was no change in expression of 4th chromosomal and heterochromatic genes. This finding is broadly comparable to reports of reduced X chromosome expression following msl2 RNAi knockdown in S2 cells. Hence MSL2 is required for up-regulation of male X chromosome where as it is not necessary for normal expression of 4th chromosomal genes and heterochromatic genes in Drosophila melanogaster males.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE12054 | GEO | 2009/08/03

SECONDARY ACCESSION(S): PRJNA113383

REPOSITORIES: GEO

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Transcription profiling of Drosophila msl21 male larvae reveals MSL2 is required for upregulation of male X chromosome but not for expression of autosomal genes

Project description:Drosophila males double transcription of their single X chromosome to equalize X-linked gene expression with females, which carry two X chromosomes. Increased transcription requires the Male-Specific Lethal (MSL) complex. The MSL2 protein is essential component of the MSL complex. MSL2 is the only protein that is strictly limited to males. MSL2 together with MSL1 forms the core of the MSL complex. The global effect of msl2 mutation on gene expression was measured by microarray analysis. We found that expression of the X chromosome was decreased in msl21 male larvae, supporting the involvement of MSL2 in the up-regulation of X-linked genes. However, there was no change in expression of 4th chromosomal and heterochromatic genes. This finding is broadly comparable to reports of reduced X chromosome expression following msl2 RNAi knockdown in S2 cells. Hence MSL2 is required for up-regulation of male X chromosome where as it is not necessary for normal expression of 4th chromosomal genes and heterochromatic genes in Drosophila melanogaster males. Experiment Overall Design: Total RNA was prepared from groups of 50 (or more in case of smaller larvae) third instar larvae by TRIzol (Invitrogen) extraction and purified using the RNeasy kit (Qiagen). Three independent RNA preparations for each genotype served as templates for probe synthesis. Affymetrix Drosophila Genome 2.0 chips were hybridized to these probes (Santa Clara, CA). Affymetrix Gene expression data was background corrected, normalized and summarized into a one expression value per sample and probeset using the RMA (robust multi-array average) algorithm. Changes in gene expression (log2 fold changes) were determined by comparing the mean RMA expression values in the msl21 sample to the mean RMA expression values in the msl21/+ samples.

2009-08-07 | E-GEOD-12054 | biostudies-arrayexpress

N-terminus of Drosophila MSL1 interacts with DNA-binding proteins and is critical for the recruitment of the dosage compensation complex to the X chromosome

Project description:The male-specific lethal dosage compensation complex (MSL complex or DCC), which consists of five proteins and two non-coding roX RNAs, is necessary for the transcriptional enhancement of X-linked genes to compensate for the sex chromosome monosomy in Drosophila XY males, compared with XX females. MSL2 is a single protein component of the DCC that is expressed only in males and is essential for the specific recruitment of the DCC to the high-affinity “entry” sites (HASs) on the X chromosome. MSL2, together with MSL1, forms the heterotetrameric DCC core. Here, we demonstrated that the N-terminal unstructured region of MSL1 interacts with many different DNA-binding proteins that contain clusters of the C2H2 zinc-finger domains. Amino acid deletions in the N-terminal region of MSL1 strongly affect the binding of the DCC to the HASs on the male X chromosome. However, the binding of MSL2 to autosomal promoters was unaffected by amino acid deletions in MSL1. Males expressing mutant variants of MSL1 died during the larvae stage, demonstrating the critical role played by the N-terminal region in DCC activity. Our results suggest that MSL1 interacts with a variety of DNA-binding proteins to increase the specificity of DCC recruitment to the male X chromosome.

2022-08-30 | GSE161128 | GEO

The interaction of MLE with CLAMP zinc finger domains is important for dosage compensation in Drosophila melanogaster

Project description:The Drosophila male-specific lethal (MSL) complex binds to the male X chromosome to activate transcription, and consists of five proteins, MSL1, MSL2, MSL3, MOF, MLE, and two roX RNAs. The MLE helicase remodels the roX lncRNAs, enabling the lncRNA-mediated assembly of the Drosophila dosage compensation complex. MSL2 is expressed only in males and interacts with the N-terminal zinc-finger of the transcription factor CLAMP that is important for specific recruitment of the MSL complex on the male X chromosome. Here we found that the unstructured C-terminal region of MLE interacts with 6-7 zinc-finger domains of CLAMP. In vitro 4-5 zinc fingers are critical for specific DNA-binding of CLAMP with GA-repeats, which constitute the core motif at the high affinity binding sites for MSL proteins. Deletion of the Clamp Binding Domain (CBD) in MLE results in decreasing of MSL proteins association with male X chromosome and increasing of male lethality. These results suggest that interactions of unstructured regions in MSL2 and MLE with CLAMP zinc finger domains are important for the specific recruitment of the MSL complex on the male X chromosome.

2024-03-20 | GSE239354 | GEO

RNA-seq of mouse ES cells depleted of MOF, MSL1, MSL2 or KANSL3

Project description:We have studied the regulatory potential of MYST1-(MOF)-containing MSL and NSL complexes in mouse embryonic stem cells (ESCs) and neuronal progenitors. We find that both complexes influence transcription by binding to promoters as well as TSS-distal enhancer regions. In contrast to flies, the MSL complex is not enriched on the X chromosome yet it is crucial for mammalian X chromosome regulation as it specifically regulates Tsix ncRNA, the major repressor of Xist lncRNA. MSL depletion leads to severely decreased Tsix expression, reduced REX1 recruitment, and consequently accumulation of Xist RNA in ESCs. The NSL complex provides additional, Tsix-independent repression of Xist by maintaining pluripotency. MSL and NSL complexes therefore act synergistically by using distinct pathways to ensure a fail-safe mechanism for the repression of X inactivation in ESCs. We have performed ChIP-seq of KANSL3, MCRS1, MOF, MSL1 and MSL2 in mouse ESCs, and KANSL3, MOF and MSL2 in NPCs, in duplicate and normalised against their inputs. We have also performed RNA-seq following knockdown of Kansl3, Mof, Msl1 and Msl2 mouse embryonic stem cells in triplicate. NB: Kansl3 and Mof knockdown-RNAseq are analyzed against their own scrambled controls, and Msl1 and Msl2 against another scrambled control triplicate.

2014-06-03 | E-GEOD-57698 | biostudies-arrayexpress

Transcriptome profiling of wild type and Pof mutant Drosophila melanogaster females

Project description:In Drosophila, two chromosome-wide compensatory systems have been characterized; the dosage compensation system acting on the male X-chromosome and the chromosome specific regulation of genes located on the heterochromatic 4th chromosome. Dosage compensation in Drosophila is accomplished by hypertranscription of the single male X-chromosome mediated by the MSL-complex. The mechanism for this compensation is suggested to be an MSL-complex mediated enhanced transcriptional elongation while the mechanism for the compensation mediated by Painting of fourth (POF) on the 4th chromosome has remained elusive. Here we show that POF binds to nascent RNA and this binding is associated with an increase in amount of chromosome 4 transcripts. Furthermore, genes located on the 4th chromosome are enriched in binding of the nucleoplasmic nucleporin component NUP98 and this enrichment correlates to increased POF binding. We also show that genes located in heterochromatic regions have a shorter transition time from site of transcription and to the nuclear envelope. Our current work broadens the understanding about how genes in heterochromatic regions can overcome the repressive influence of their hostile environment. Pof mutant vs. wild type, 3 replicates

2012-05-30 | E-GEOD-28513 | biostudies-arrayexpress

Genome-wide profiling of RNA associated to the chromosome 4 specific protein POF in Drosophila melanogaster

2012-05-31 | GSE28518 | GEO

Transcriptome profiling of wild type and Pof mutant Drosophila melanogaster females

2012-05-31 | GSE28513 | GEO

ChIP-seq of MOF, MSL and NSL complex members in mouse ES cells and neuronal progenitors

Project description:We assessed the genome-wide binding of the histone acetylase MOF and members of its two associated complexes, the male-specific lethal and the non-specific lethal complex (MSL, NSL). We generated ChIP-seq profiles for MOF, MSL1, MSL2, KANSL3, and MCRS1 from mouse embryonic stem cells and neuronal progenitor cells. By using two replicates per sample and stringent filtering criteria, we identify five basic groups of genome regions where the proteins show either mutual or exclusive binding. We find that the NSL complex members (KANSL3, MCRS1) target the TSSs of broadly expressed genes with housekeeping functions in both cell types. MOF and particularly the MSL complex target a subset of these NSL-complex-targets, too. In addition, we find several thousand TSS-distal binding sites, particularly in ESCs, where KANSL3, MSL2 and MCRS1 show strong enrichments for annotated ESC enhancers. The vast majority of the binding to these ESC distal regulatory elements is lost in NPCs. Finally, we identify mostly intronic and intergenic regions with predominant MSL2 enrichments without the presence of its known interactors. These binding sites do not overlap with ESC marks of active chromatin (e.g. DNase hypersensitivity sites), but the they increase in number upon differentiation and we detect a strong signature of the (CAGA)n motif. Our study provides the first comprehensive analysis of MOF in the context of its two complexes in the mouse and reveals shared as well as distinct and dynamic functions for gene regulation and pluripotency. ChIP-seq of MOF and members of its associated complexes (MSL complex: MSL1, MSL2; NSL complex: KANSL3, MCRS1) in male mouse embryonic stem cells and neuronal progenitor cells derived from them.

2014-06-03 | E-GEOD-51746 | biostudies-arrayexpress

roX RNAs are required for up-regulation of male X chromosome in Drosophila.

Project description:Drosophila males double transcription of their single X chromosome to equalize X-linked gene expression with females, which carry two X chromosomes. Increased transcription requires the Male-Specific Lethal (MSL) complex. One of the primary functions of the MSL complex is thought to be enrichment of H4Ac16 on the male X chromosome, a modification linked to elevated transcription. The roX1 and roX2 RNAs are essential but redundant components of the MSL complex. Simultaneous removal of both roX RNAs reduces MSL X-localization and leads to ectopic binding of these proteins at autosomal sites and to the chromocenter. Some H4Ac16 accumulates at these ectopic sites in roX1- roX2- males, suggesting the possibility of increased expression. The global effect of roX mutations on gene expression was measured by microarray analysis. We found that expression of the X chromosome was decreased by 26% in roX1- roX2- male larvae, supporting the involvement of roX RNAs in the up-regulation of X-linked genes. This finding is broadly comparable to reports of reduced X chromosome expression following msl2 RNAi knockdown in S2 cells. In spite of strong MSL binding and H4Ac16 accumulation at autosomal sites in roX1- roX2- males, enhanced gene expression could not be detected at these sites by microarray analysis or reverse northern blotting. Thus, failure to compensate X-linked genes, rather than inappropriate up-regulation of autosomal genes at ectopic sites of MSL binding, appears to cause male lethality upon loss of roX RNAs. Keywords: effect of roX1-roX2- mutant on gene expression

2007-01-06 | GSE3990 | GEO

Genome-wide profiling of RNA associated to the MSL-complex in Drosophila melanogaster

Project description:In Drosophila, the global increase in transcription from the X chromosome in males to compensate for its monosomy is mediated by the male-specific-lethal complex (MSL-C) consisting of five proteins and two non-coding RNAs, roX1 and roX2. After an initial sequence dependent recognition by the MSL-C of 150-300 high affinity sites, the spreading to the majority of the X-linked genes depends on local MSL-C concentration and active transcription. Here we ask whether any additional RNA species are associated to the MSL-C. No additional roX were found but a strong association was found between the msl2 mRNA and the MSL-C. Based on our results we propose a model in which a non-chromatin associated partial or complete MSL-C titrates newly transcribed msl2 mRNA and thus feed-back regulates the amount of available MSL-C. In total 12 samples; 4 Input files (4 different conditions) with the corresponding 8 RIP samples (2 different antibodies, same 4 conditions as Input)

2011-04-13 | E-GEOD-20249 | biostudies-arrayexpress

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