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Correct dosage of X chromosome transcription is controlled by a nuclear pore component

ABSTRACT: Correct dosage of X chromosome transcription is controlled by a nuclear pore component

PROVIDER: PRJNA649320 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12341561_1.fastq.gz	Fastqsanger.gz
	SRR12341561_2.fastq.gz	Fastqsanger.gz
	SRR12341562_1.fastq.gz	Fastqsanger.gz
	SRR12341562_2.fastq.gz	Fastqsanger.gz
	SRR12341563_1.fastq.gz	Fastqsanger.gz

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Correct dosage of X chromosome transcription is controlled by a nuclear pore component

Project description:We show that a nuclear pore component, Mtor, is involved in setting the correct levels of transcription from the male X chromosome. Using larval tissues, we demonstrate that depletion of Mtor results in selective upregulation at MSL targets of the male X, beyond the required two-fold. Mtor and MSL components interact genetically, and depletion of Mtor can rescue the male lethality phenotype of MSL components. Using RNA FISH analysis and nascent transcript sequencing, we find that Mtor’s effect is not due to defects in mRNA export, but occurs at the level of nascent transcription.

2021-06-15 | GSE155323 | GEO

Correct dosage of X chromosome transcription is controlled by a nuclear pore component.

Project description:Dosage compensation in Drosophila melanogaster involves a 2-fold transcriptional upregulation of the male X chromosome, which relies on the X-chromosome-binding males-specific lethal (MSL) complex. However, how such 2-fold precision is accomplished remains unclear. Here, we show that a nuclear pore component, Mtor, is involved in setting the correct levels of transcription from the male X chromosome. Using larval tissues, we demonstrate that the depletion of Mtor results in selective upregulation at MSL targets of the male X, beyond the required 2-fold. Mtor and MSL components interact genetically, and depletion of Mtor can rescue the male lethality phenotype of MSL components. Using RNA fluorescence in situ hybridization (FISH) analysis and nascent transcript sequencing, we find that the effect of Mtor is not due to defects in mRNA export but occurs at the level of nascent transcription. These findings demonstrate a physiological role for Mtor in the process of dosage compensation, as a transcriptional attenuator of X chromosome gene expression.

| S-EPMC8224986 | biostudies-literature

Nuclear pore component Nup155 is part of the p53 network in liver cancer

Project description:Cancer-relevant signalling pathways rely on bidirectional nucleocytoplasmic transport events through the nuclear pore complex (NPC). However, mechanisms by which individual NPC components (Nups) participate in the regulation of these pathways remain poorly understood. We discovered by integrating large scale proteomics, polysome fractionation and a focused RNAi approach that Nup155 controls mRNA translation of p21 (CDKN1A), a key mediator of the p53 response. The underlying mechanism involves transcriptional regulation of the putative tRNA and rRNA methyltransferase FTSJ1 by Nup155. Furthermore, we observed that Nup155 and FTSJ1 are p53 repression targets and accordingly found a correlation between the p53 status, Nup155 and FTSJ1 expression in murine and human hepatocellular carcinoma (HCC). Our data suggest an unanticipated regulatory network linking translational control by and repression of a structural NPC component modulating the p53 pathway through its effectors.

2019-04-09 | PXD012373 | Pride

Effect of nuclear pore complex (NPC) blockage by WGA treatment on zygotic genome activation (ZGA) during zebrafish early development

Project description:To investigate the function of nuclear pore complex (NPC) in the regulation of zygotic genome activation (ZGA), we microinjected medium dosage of WGA in zebrafish embryos at 1-cell stage to block NPC function. We then performed gene expression profiling analysis using data obtained from RNA-seq of control or WGA treated embryo at comparable developmental time point (4.3 hours post fertilization (hpf) ) or develomental stage (dome).

2023-02-22 | GSE212929 | GEO

Wnt signaling dosage controlled by a Ctnnb1 enhancer balances homeostasis and tumorigenesis of intestinal epithelia

Project description:Wnt signaling dosage controlled by a Ctnnb1 enhancer balances homeostasis and tumorigenesis of intestinal epithelia

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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

Distal and proximal cis-regulatory elements sense X-dosage and developmental state at the Xist locus

Project description:Developmental genes such as Xist, the master regulator of X-chromosome inactivation (XCI), are controlled by complex cis-regulatory landscapes, which decode multiple signals to establish specific spatio-temporal expression patterns. Xist integrates information on X-chromosomal dosage and developmental stage to trigger XCI at the primed pluripotent state in females only. Through a pooled CRISPR interference screen in differentiating mouse embryonic stem cells, we identify functional enhancer elements of Xist during the onset of random XCI. By quantifying how enhancer activity is modulated by X-dosage and differentiation, we find that X-dosage controls the promoter-proximal region in a binary switch-like manner. By contrast, differentiation cues activate a series of distal elements and bring them into closer spatial proximity of the Xist promoter. The strongest distal element is part of an enhancer cluster ~200 kb upstream of the Xist gene which is associated with a previously unannotated Xist-enhancing regulatory transcript, we named Xert. Developmental cues and X-dosage are thus decoded by distinct regulatory regions, which cooperate to ensure female-specific Xist upregulation at the correct developmental time. Our study is the first step to disentangle how multiple, functionally distinct regulatory regions interact to generate complex expression patterns in mammals.

2021-03-04 | GSE167358 | GEO

Binding of the C. elegans dosage compensation complex protein DPY-27

Project description:Dosage Compensation is required to correct for uneven gene dose between the sexes. We utilized global run-on sequencing (GRO-seq) to examine how Caenorhabditis elegans dosage compensation reduces transcription of X-linked genes. To facilitate these experiments, we required accurate 5’-ends of genes that have been missing due to a co-transcriptional trans-splicing event common in nematodes. We developed a modified GRO-seq protocol to identify TSSs that are supported by transcription, and determined that TSSs lie more than 1 kb upstream of the previously annotated TSS for nearly one-quarter of all genes. We then investigated the changes that occur in transcriptionally engaged RNA Polymerase when dosage compensation is disrupted, and find that dosage compensation controls recruitment of RNA Polymerase to X-linked genes.

2013-06-18 | GSE43086 | GEO

Chromatin proteins linked to dosage compensation in Drosophila captured by ChIP-mass spectrometry

Project description:We report the usage of ChIP-mass spectrometry in identifying proteins and histone modifications involved in Drosophila dosage compensation. We identified a chromatin targeting factor, CG4747, that is involved in recognition of H3K36me3 and robust recruitment of the Drosophila MSL complex to its correct targets on the male X chromosome.

2012-11-06 | GSE42025 | GEO

Binding of the C. elegans dosage compensation complex protein DPY-27

Project description:Dosage Compensation is required to correct for uneven gene dose between the sexes. We utilized global run-on sequencing (GRO-seq) to examine how Caenorhabditis elegans dosage compensation reduces transcription of X-linked genes. To facilitate these experiments, we required accurate 5M-bM-^@M-^Y-ends of genes that have been missing due to a co-transcriptional trans-splicing event common in nematodes. We developed a modified GRO-seq protocol to identify TSSs that are supported by transcription, and determined that TSSs lie more than 1 kb upstream of the previously annotated TSS for nearly one-quarter of all genes. We then investigated the changes that occur in transcriptionally engaged RNA Polymerase when dosage compensation is disrupted, and find that dosage compensation controls recruitment of RNA Polymerase to X-linked genes. Two biological replicates of ChIP with DPY-27 and a random rabbit IgG

2013-06-18 | E-GEOD-43086 | biostudies-arrayexpress

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