Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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

PROVIDER: PRJNA675621 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

N-terminus of Drosophila MSL1 is critical for dosage compensation

Project description:N-terminus of Drosophila MSL1 is critical for dosage compensation

| PRJNA1018430 | ENA

N-terminus of Drosophila MSL1 is critical for dosage compensation

Project description:The male-specific dosage compensation complex (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. The MSL1 and MSL2 proteins form the heterotetrameric core of DCC and are critical for the specific recruitment of the DCC to the high-affinity “entry” sites (HAS) on the X chromosome. Here we demonstrated that the N-terminal region of MSL1 is critical for its stability and functions. Amino acid deletions and substitutions in the N-terminal region of MSL1 strongly affect both interaction with roX2 RNA and DCC binding to HAS on the X chromosome. In particular, substitution of the conserved N-terminal amino-acids 3-7 in MSL1GS has an affect on dosage compensation similar to inactivation of genes encoding roX RNAs. MSL1GS binds to promoters like MSL1WT but does not co-bind with MSL2 and MSL3 to X chromosomal HAS. However, over-expression of MSL2 partially restores the functional activity of MSL1GS in dosage compensation. Thus, the interaction of MSL1 with roX RNA is critical for the efficient assembly of DCCs on HAS of the male X chromosome.

2024-11-30 | GSE243396 | GEO

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

Dosage compensation mass spectrometry in platypus, chicken and mouse

Project description:Gene dosage imbalance of heteromorphic sex chromosomes (XY or ZW) exists between the sexes, and with the autosomes. Mammalian X chromosome inactivation was long thought to imply a critical need for dosage compensation in vertebrates. However, mRNA abundance measurements that demonstrated sex chromosome transcripts are neither balanced between the sexes or with autosomes in monotreme mammals or birds brought sex chromosome dosage compensation into question. This study examines transcriptomic and proteomic levels of dosage compensation in platypus and chicken compared to mouse, a model eutherian species. We analyzed mRNA and protein levels in heart and liver tissues of chicken, mouse and platypus.

2024-07-30 | PXD040182 | Pride

The activation potential of MOF is constrained for dosage compensation

Project description:The H4K16 acetyltransferase MOF plays a crucial role in dosage compensation in Drosophila, but has additional, global functions. We compared the molecular context and effect of MOF in male and female flies combining chromosome-wide mapping and transcriptome studies with analyses of defined reporter loci in transgenic flies. MOF distributes dynamically between two complexes, the Dosage Compensation Complex and a complex containing MBD-R2, a global facilitator of transcription. These different targeting principles define the distribution of MOF between the X chromosome and autosomes and at transcription units with 5’ or 3’ enrichment. The male X chromosome differs from all other chromosomes in that H4K16 acetylation levels do not correlate with transcription output. The reconstitution of this phenomenon at a model locus revealed that the activation potential of MOF is constraint in male cells in the context of the DCC to arrive at the two-fold activation of transcription characteristic of dosage compensation. ChIP-chip profiling of MBD-R2, MOF and MSL1 in adult male and female flies, and SL2 cells, incl. at least 3 biological replicates

2010-06-26 | E-GEOD-20695 | biostudies-arrayexpress

Trisomy 21 Dosage Compensation Map (T21DoCoMap)

Project description:Trisomy 21 Dosage Compensation Map (T21DoCoMap)

| PRJNA720724 | ENA

Trisomy 21 Dosage Compensation Map (T21DoCoMap)

Project description:Trisomy 21 Dosage Compensation Map (T21DoCoMap)

| PRJNA720725 | ENA

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 stability controlled by m6A methylation contributes to X-to-autosome dosage compensation in mammals

Project description:In mammals, X-chromosomal genes are expressed from a single copy since males (XY) possess a single X chromosome, while females (XX) undergo X inactivation. To compensate for this reduction in dosage compared to two active copies of autosomes, it has been proposed that genes from the active X chromosome exhibit dosage compensation. However, the existence and mechanism of X-to-autosome dosage compensation are still under debate. Here, we show that X-chromosomal transcripts are reduced in m6A modifications and more stable compared to their autosomal counterparts. Acute depletion of m6A selectively stabilises autosomal transcripts, resulting in perturbed dosage compensation in mouse embryonic stem cells. We propose that higher stability of X-chromosomal transcripts is directed by lower levels of m6A, indicating that mammalian dosage compensation is partly regulated by epitranscriptomic RNA modifications.

| EGAS00001007112 | EGA

Developmental dynamics of C. elegans dosage compensation

Project description:Developmental dynamics of C. elegans dosage compensation

| PRJNA280541 | ENA