scholarly journals Differential Occupancy of Two GA-Binding Proteins Promotes Targeting of the Drosophila Dosage Compensation Complex to the Male X Chromosome

Cell Reports ◽  
2018 ◽  
Vol 22 (12) ◽  
pp. 3227-3239 ◽  
Author(s):  
Emily G. Kaye ◽  
Matthew Booker ◽  
Jesse V. Kurland ◽  
Alexander E. Conicella ◽  
Nicolas L. Fawzi ◽  
...  
Keyword(s):  
X Chromosome ◽  
Dosage Compensation ◽  
Binding Proteins ◽  
Dosage Compensation Complex

scholarly journals 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

2020 ◽  
Author(s):  
Valentin Babosha ◽  
Natalia Klimenko ◽  
Evgeniya Tikhonova ◽  
Alexander Shilovich ◽  
Pavel Georgiev ◽  
...  
Keyword(s):  
Amino Acid ◽  
Dna Binding ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Binding Proteins ◽  
Dna Binding Proteins ◽  
Terminal Region ◽  
Dosage Compensation Complex ◽  
N Terminus ◽  
Msl Complex

ABSTRACTThe 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.BulletsThe N-terminal region of MSL1 interacts with 14 C2H2-type zinc-finger DNA-binding proteinsThe N-terminus of MSL1 is critical for the specific recruitment of the MSL complex to the X chromosomeThe N-terminus of MSL1 is important for the binding of MSL2 to a small fraction of autosomal promoters

scholarly journals Msl1-Mediated Dimerization of the Dosage Compensation Complex Is Essential for Male X-Chromosome Regulation in Drosophila

2012 ◽  
Vol 48 (4) ◽  
pp. 587-600 ◽  
Author(s):  
Erinc Hallacli ◽  
Michael Lipp ◽  
Plamen Georgiev ◽  
Clare Spielman ◽  
Stephen Cusack ◽  
...  
Keyword(s):  
X Chromosome ◽  
Dosage Compensation ◽  
Dosage Compensation Complex

scholarly journals The DNA binding CXC domain of MSL2 is required for faithful targeting the Dosage Compensation Complex to the X chromosome

2010 ◽  
Vol 38 (10) ◽  
pp. 3209-3221 ◽  
Author(s):  
Torsten Fauth ◽  
Felix Müller-Planitz ◽  
Cornelia König ◽  
Tobias Straub ◽  
Peter B. Becker
Keyword(s):  
Dna Binding ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Dosage Compensation Complex

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 The Caenorhabditis elegans Dosage Compensation Machinery Is Recruited to X Chromosome DNA Attached to an Autosome

Genetics ◽  
2000 ◽  
Vol 156 (4) ◽  
pp. 1603-1621
Author(s):  
Jason D Lieb ◽  
Carlos Ortiz de Solorzano ◽  
Enrique Garcia Rodriguez ◽  
Arthur Jones ◽  
Michael Angelo ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Dna Sequences ◽  
Three Dimensional ◽  
Dosage Compensation Complex ◽  
X Chromosomes ◽  
Cis Acting ◽  
Recognition Elements ◽  
The Right

Abstract The dosage compensation machinery of Caenorhabditis elegans is targeted specifically to the X chromosomes of hermaphrodites (XX) to reduce gene expression by half. Many of the trans-acting factors that direct the dosage compensation machinery to X have been identified, but none of the proposed cis-acting X chromosome-recognition elements needed to recruit dosage compensation components have been found. To study X chromosome recognition, we explored whether portions of an X chromosome attached to an autosome are competent to bind the C. elegans dosage compensation complex (DCC). To do so, we devised a three-dimensional in situ approach that allowed us to compare the volume, position, and number of chromosomal and subchromosomal bodies bound by the dosage compensation machinery in wild-type XX nuclei and XX nuclei carrying an X duplication. The dosage compensation complex was found to associate with a duplication of the right 30% of X, but the complex did not spread onto adjacent autosomal sequences. This result indicates that all the information required to specify X chromosome identity resides on the duplication and that the dosage compensation machinery can localize to a site distinct from the full-length hermaphrodite X chromosome. In contrast, smaller duplications of other regions of X appeared to not support localization of the DCC. In a separate effort to identify cis-acting X recognition elements, we used a computational approach to analyze genomic DNA sequences for the presence of short motifs that were abundant and overrepresented on X relative to autosomes. Fourteen families of X-enriched motifs were discovered and mapped onto the X chromosome.

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.

Sex-Specific Assembly of a Dosage Compensation Complex on the Nematode X Chromosome

Science ◽  
1996 ◽  
Vol 274 (5293) ◽  
pp. 1736-1739 ◽  
Author(s):  
P.-T. Chuang ◽  
J. D. Lieb ◽  
B. J. Meyer
Keyword(s):  
X Chromosome ◽  
Dosage Compensation ◽  
Dosage Compensation Complex
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