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MSL2 reads DNA shape to distinguish X from autosome for dosage compensation

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE75033 | GEO | 2016/08/30

SECONDARY ACCESSION(S): PRJNA302262

REPOSITORIES: GEO

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MSL2 reads DNA shape to distinguish X from autosome for dosage compensation (DIP experiments)

Project description:The rules according to which transcription factors selectively bind only a small subset of genomic sites from a vast pool of similar sequences are not understood. One of the most challenging tasks in DNA recognition is posed by dosage compensation systems that require the unequivocal distinction between a sex chromosome and all autosomes. In Drosophila melanogaster the male-specific-lethal dosage compensation complex (MSL-DCC) doubles the transcription output of most genes on the X chromosome via chromatin modification, but the nature of this selectivity is not known. We now found that MSL2, the male-specific organizer of the DCC, uses two distinct DNA interaction surfaces to read out previously identified X chromosomal ‘high affinity sites’. Specificity is provided by the interaction of the CXC domain with a novel, X-specific motif defined by DNA sequence and shape features. By several criteria these ‘PionX sites’ are primary determinants of X chromosome identity.

2016-08-30 | GSE75030 | GEO

MSL2 reads DNA shape to distinguish X from autosome for dosage compensation (MLE RNAi in S2 cells experiments)

2016-08-30 | GSE75032 | GEO

MSL2 reads DNA shape to distinguish X from autosome for dosage compensation (SXL RNAi in Kc cells experiments)

2016-08-30 | GSE75031 | GEO

MSL2 reads DNA shape to distinguish X from autosome for dosage compensation

Project description:MSL2 reads DNA shape to distinguish X from autosome for dosage compensation

| PRJNA302262 | ENA

Structural basis of X chromosome DNA recognition by the MSL2 CXC domain during Drosophila dosage compensation.

Project description:The male-specific lethal dosage compensation complex (MSL-DCC) selectively assembles on the X chromosome in Drosophila males and activates gene transcription by twofold through histone acetylation. An MSL recognition element (MRE) sequence motif nucleates the initial MSL association, but how it is recognized remains unknown. Here, we identified the CXC domain of MSL2 specifically recognizing the MRE motif and determined its crystal structure bound to specific and nonspecific DNAs. The CXC domain primarily contacts one strand of DNA duplex and employs a single arginine to directly read out dinucleotide sequences from the minor groove. The arginine is flexible when bound to nonspecific sequences. The core region of the MRE motif harbors two binding sites on opposite strands that can cooperatively recruit a CXC dimer. Specific DNA-binding mutants of MSL2 are impaired in MRE binding and X chromosome localization in vivo. Our results reveal multiple dynamic DNA-binding modes of the CXC domain that target the MSL-DCC to X chromosomes.

| S-EPMC4248295 | biostudies-literature

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

Project description:Dosage compensation in Drosophila melanogaster involves the selective targeting of the male X chromosome by the dosage compensation complex (DCC) and the coordinate, approximately 2-fold activation of most genes. The principles that allow the DCC to distinguish the X chromosome from the autosomes are not understood. Targeting presumably involves DNA sequence elements whose combination or enrichment mark the X chromosome. DNA sequences that characterize 'chromosomal entry sites' or 'high-affinity sites' may serve such a function. However, to date no DNA binding domain that could interpret sequence information has been identified within the subunits of the DCC. Early genetic studies suggested that MSL1 and MSL2 serve to recognize high-affinity sites (HAS) in vivo, but a direct interaction of these DCC subunits with DNA has not been studied. We now show that recombinant MSL2, through its CXC domain, directly binds DNA with low nanomolar affinity. The DNA binding of MSL2 or of an MSL2-MSL1 complex does not discriminate between different sequences in vitro, but in a reporter gene assay in vivo, suggesting the existence of an unknown selectivity cofactor. Reporter gene assays and localization of GFP-fusion proteins confirm the important contribution of the CXC domain for DCC targeting in vivo.

| S-EPMC2879509 | biostudies-literature

MSL2 is an allelic dosage sensor in mammals

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-08-10 | GSE183556 | GEO

Differential Chromatin Binding of the Drosophila Dosage Compensation Complex

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2012-12-11 | E-GEOD-37865 | biostudies-arrayexpress

RNA stability controlled by m6A methylation provides X to autosome compensation in mammals

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-02-14 | GSE203653 | GEO

RNA stability controlled by m<sup>6</sup>A 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 with two active copies of autosomes, it has been proposed that genes from the active X chromosome exhibit dosage compensation. However, the existence and mechanisms of X-to-autosome dosage compensation are still under debate. Here we show that X-chromosomal transcripts have fewer m6A modifications and are more stable than their autosomal counterparts. Acute depletion of m6A selectively stabilizes 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.

| S-EPMC10442230 | biostudies-literature

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