scholarly journals Enriched G-quadruplexes on the Drosophila Male X Chromosome Function as Insulators of Dosage Compensation Complex

2019 ◽  
Author(s):  
Sheng-Hu Qian ◽  
Lu Chen ◽  
Zhen-Xia Chen
Keyword(s):  
Y Chromosome ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Binding Sites ◽  
Fine Tuning ◽  
Dosage Compensation Complex ◽  
Evolutionary Trajectory ◽  
Male Specific ◽  
Flanking Regions ◽  
Y Chromosome Degeneration

AbstractThe evolution of sex chromosomes has resulted in half X chromosome dosage in males as females. Dosage compensation, or the two-fold upregulation in males, was thus evolved to balance the gene expression between sexes. However, the step-wise evolutionary trajectory of dosage compensation during Y chromosome degeneration is still unclear. Here, we show that the specific structured elements G-quadruplexes (G4s) are enriched on the X chromosome in Drosophila melanogaster. Meanwhile, on the X chromosome, the G4s are underrepresented on the H4K16 acetylated regions and the binding sites of dosage compensation complex male-specific lethal (MSL) complex. Peaks of G4 density and potential are observed at the flanking regions of MSL binding sites, suggesting G4s act as insulators to precisely up-regulate certain regions in males. Thus, G4s may be involved in the evolution of dosage compensation process through fine-tuning one-dose proto-X chromosome regions around MSL binding sites during the gradual Y chromosome degeneration.One Sentence SummaryG-quadruplexes act as insulators to precisely up-regulate X chromosome in males.

scholarly journals GA-repeats on mammalian X chromosomes support Ohno’s hypothesis of dosage compensation by transcriptional upregulation

2018 ◽  
Author(s):  
Edridge D’Souza ◽  
Elizaveta Hosage ◽  
Kathryn Weinand ◽  
Steve Gisselbrecht ◽  
Vicky Markstein ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transposable Elements ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Binding Sites ◽  
Convergent Evolution ◽  
Fruit Fly ◽  
Dosage Compensation Complex ◽  
X Chromosomes ◽  
Repeat Sequences

ABSTRACTOver 50 years ago, Susumo Ohno proposed that dosage compensation in mammals would require upregulation of gene expression on the single active X chromosome, a mechanism which to date is best understood in the fruit fly Drosophila melanogaster. Here, we report that the GA-repeat sequences that recruit the conserved MSL dosage compensation complex to the Drosophila X chromosome are also enriched across mammalian X chromosomes, providing genomic support for the Ohno hypothesis. We show that mammalian GA-repeats derive in part from transposable elements, suggesting a mechanism whereby unrelated X chromosomes from dipterans to mammals accumulate binding sites for the MSL dosage compensation complex through convergent evolution, driven by their propensity to accumulate transposable elements.

scholarly journals Interactions between dosage compensation complex components Msl-1, Msl-2 and NURF component NURF301 with long non-coding RNA gene hsrω

2019 ◽  
Author(s):  
Deo Prakash Chaturvedi
Keyword(s):  
X Chromosome ◽  
Dosage Compensation ◽  
Dosage Compensation Complex ◽  
Chromatin Remodeler ◽  
Down Regulation ◽  
Over Expression ◽  
Non Coding Rna ◽  
Crucial Component ◽  
Male Specific ◽  
Long Non Coding Rna

AbstractHyperactivity of the single X-chromosome in male Drosophila is achieved by establishing a ribonucleoprotein complex, called Dosage Compensation Complex (DCC), on the male X chromosome. Msl-1 and Msl-2 proteins, involved in the initiation and establishing of DCC on male X chromosome, are very crucial component of this complex. In the present study, it has been found here that a long non-coding RNA gene hsrω genetically interacts with Msl-1 as well as Msl-2 and suppresses the lethal phenotype of Msl-1 or Msl-2 down-regulation in its up-regulated background. Additionally, it is also found here that an ATP-dependent chromatin remodeler, NURF301, also interacts with hsrω in same manner. General lethality caused by Act-GAL4 driven global expression of NURF301-RNAi and the male-specific lethality following Msl-1-RNAi or Msl-2-RNAi transgene expression were partially suppressed by over-expression of hsrω, but not by down regulation through hsrω-RNAi. Likewise, eye phenotypes following ey-GAL4 driven down-regulation of NURF301 or Msl-1 or Msl-2 were also partially suppressed by over-expression of hsrω. Act-GAL4 driven global over-expression of hsrω along with Msl-1-RNAi or Msl-2-RNAi transgene substantially restored levels of MSL-2 protein on the male X chromosome. Similarly, levels and distribution of Megator protein, which was reduced and distribution at nuclear rim and in nucleoplasm was affected in the MT and SG nuclei, is also restored when hsrω transcripts are down-regulated in Act-GAL4 driven Msl-1-RNAi or Msl-2-RNAi genetic background. NURF301, a known chromatin remodeler, when down-regulated shows decondensed X chromosome in male larvae. Down-regulation of hsrω results in restoration of chromosome architecture without affecting the level of ISWI protein-another chromatin remodeler protein, known to interacting with hsrω.

scholarly journals Targeting of the dosage-compensated male X-chromosome during early Drosophila development

2019 ◽  
Author(s):  
LE Rieder ◽  
WT Jordan ◽  
EN Larschan
Keyword(s):  
Early Development ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Binding Sites ◽  
Zinc Finger Protein ◽  
Multi Stage ◽  
Compensation Factor ◽  
Zygotic Transcription ◽  
Male Specific ◽  
Lethal Dosage

ABSTRACTThe essential process of dosage compensation, which corrects for the imbalance in X-linked gene expression between XX females and XY males, represents a key model for how genes are targeted for coordinated regulation. However, the mechanism by which dosage compensation complexes identify the X-chromosome during early development remained unknown because of the difficulty of sexing embryos prior to zygotic transcription. We used meiotic drive to sex Drosophila embryos prior to zygotic transcription and ChIP-seq to measure dynamics of dosage compensation factor targeting. The Drosophila Male-Specific Lethal dosage compensation complex (MSLc) requires the ubiquitous zinc-finger protein Chromatin-Linked Adaptor for MSL Proteins (CLAMP) to identify the X-chromosome. We observe a multi-stage process in which MSLc first identifies CLAMP binding sites throughout the genome followed by concentration at the strongest X-linked MSLc sites. We provide insight into the dynamic mechanism by which a large transcription complex identifies its binding sites during early development.

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.

scholarly journals Jil-1, a Chromosomal Kinase Implicated in Regulation of Chromatin Structure, Associates with the Male Specific Lethal (Msl) Dosage Compensation Complex

2000 ◽  
Vol 149 (5) ◽  
pp. 1005-1010 ◽  
Author(s):  
Ye Jin ◽  
Yanming Wang ◽  
Jørgen Johansen ◽  
Kristen M. Johansen
Keyword(s):  
Signal Transduction ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Chromatin Structure ◽  
Ectopic Expression ◽  
Signal Transduction Pathways ◽  
Dosage Compensation Complex ◽  
Male Specific Lethal ◽  
Msl Complex ◽  
Male Specific

JIL-1 is a novel chromosomal kinase that is upregulated almost twofold on the male X chromosome in Drosophila. Here we demonstrate that JIL-1 colocalizes and physically interacts with male specific lethal (MSL) dosage compensation complex proteins. Furthermore, ectopic expression of the MSL complex directed by MSL2 in females causes a concomitant upregulation of JIL-1 to the female X that is abolished in msl mutants unable to assemble the complex. Thus, these results strongly indicate JIL-1 associates with the MSL complex and further suggests JIL-1 functions in signal transduction pathways regulating chromatin structure.

scholarly journals Absence of X-chromosome dosage compensation in the primordial germ cells of Drosophila embryos

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ryoma Ota ◽  
Makoto Hayashi ◽  
Shumpei Morita ◽  
Hiroki Miura ◽  
Satoru Kobayashi
Keyword(s):  
X Chromosome ◽  
Germ Cells ◽  
Dosage Compensation ◽  
Sex Chromosome ◽  
Primordial Germ Cells ◽  
Histone H4 ◽  
X Chromosomes ◽  
Essential Components ◽  
Msl Complex ◽  
Male Specific

AbstractDosage compensation is a mechanism that equalizes sex chromosome gene expression between the sexes. In Drosophila, individuals with two X chromosomes (XX) become female, whereas males have one X chromosome (XY). In males, dosage compensation of the X chromosome in the soma is achieved by five proteins and two non-coding RNAs, which assemble into the male-specific lethal (MSL) complex to upregulate X-linked genes twofold. By contrast, it remains unclear whether dosage compensation occurs in the germline. To address this issue, we performed transcriptome analysis of male and female primordial germ cells (PGCs). We found that the expression levels of X-linked genes were approximately twofold higher in female PGCs than in male PGCs. Acetylation of lysine residue 16 on histone H4 (H4K16ac), which is catalyzed by the MSL complex, was undetectable in these cells. In male PGCs, hyperactivation of X-linked genes and H4K16ac were induced by overexpression of the essential components of the MSL complex, which were expressed at very low levels in PGCs. Together, these findings indicate that failure of MSL complex formation results in the absence of X-chromosome dosage compensation in male PGCs.

The msl-2 dosage compensation gene of Drosophila encodes a putative DNA-binding protein whose expression is sex specifically regulated by Sex-lethal

Development ◽  
1995 ◽  
Vol 121 (10) ◽  
pp. 3245-3258 ◽  
Author(s):  
G.J. Bashaw ◽  
B.S. Baker
Keyword(s):  
Dna Binding ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Ring Finger ◽  
The Other ◽  
Male Specific Lethal ◽  
Alternatively Spliced ◽  
Sex Lethal ◽  
Specific Regulation ◽  
Male Specific

In Drosophila dosage compensation increases the rate of transcription of the male's X chromosome and depends on four autosomal male-specific lethal genes. We have cloned the msl-2 gene and shown that MSL-2 protein is co-localized with the other three MSL proteins at hundreds of sites along the male polytene X chromosome and that this binding requires the other three MSL proteins. msl-2 encodes a protein with a putative DNA-binding domain: the RING finger. MSL-2 protein is not produced in females and sequences in both the 5′ and 3′ UTRs are important for this sex-specific regulation. Furthermore, msl-2 pre-mRNA is alternatively spliced in a Sex-lethal-dependent fashion in its 5′ UTR.

scholarly journals Multiple Classes of MSL Binding Sites Target Dosage Compensation to the X Chromosome of Drosophila

2004 ◽  
Vol 14 (6) ◽  
pp. 481-487 ◽  
Author(s):  
Hyangyee Oh ◽  
James R Bone ◽  
Mitzi I Kuroda
Keyword(s):  
X Chromosome ◽  
Dosage Compensation ◽  
Binding Sites ◽  
Target Dosage
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