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Homo sapiens

ABSTRACT: Next Generation Sequencing identifying the dosage compensation state in human endometrial carcinoma and adjacent tissues

OTHER RELATED OMICS DATASETS IN: E-GEOD-56087

PROVIDER: PRJNA242387 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1200850_1.fastq.gz	Fastqsanger.gz
	SRR1200850_2.fastq.gz	Fastqsanger.gz
	SRR1200860_1.fastq.gz	Fastqsanger.gz
	SRR1200860_2.fastq.gz	Fastqsanger.gz
	SRR1200870_1.fastq.gz	Fastqsanger.gz

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E-GEOD-56087

Project description:Next Generation Sequencing identifying the dosage compensation state in human endometrial carcinoma and adjacent tissues

2019-05-14 | E-GEOD-56087 | ExpressionAtlas

Next Generation Sequencing identifying the dosage compensation state in human endometrial carcinoma and adjacent tissues

Project description:Mammals have evolved an XY sex chromosome system, resulting in dosage imbalance not only between sexes, but also between X-chromosome and autosome. mRNA profiles of 9 pairs of human endometrial carcinoma and adjacent tissues were generated by Illumina 100-nucleotide paired-end sequencing

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RNA stability controlled by m6A methylation provides X to autosome compensation in mammals [miCLIP2]

Project description:In therian mammals, X-chromosomal genes are expressed only from a single active X chromosome, both in males (XY) as well as females (XX). To compensate for this reduction in dosage compared to the evolutionary ancestral state on two autosomes, it has been proposed that genes from the active X chromosome exhibit dosage compensation (“Ohno’s hypothesis”). However, the existence and mechanism of X-to-autosome dosage compensation are still under debate. Here, we show that dosage compensation is achieved via differential N6-methyladenosine (m6A) RNA modification. X-chromosomal transcripts are reduced in m6A modifications and more stable compared to the autosomal counterparts. Acute depletion of m6A using a small molecule inhibitor differentially affects autosomal and X-chromosomal transcripts across sexes, cell types, tissues and species, resulting in perturbed dosage compensation. We propose that higher stability of X-chromosomal transcripts is directed by lower levels of m6A, indicating that mammalian dosage compensation occurs via epitranscriptomic RNA regulation.

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RNA stability controlled by m6A methylation provides X to autosome compensation in mammals [SLAM-seq]

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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.

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Retrospective gene expression analysis of human RNA samples from Hepatocellular Carcinoma in relation with survival

Project description:The aim of this study is to identify by Next Generation Sequencing - RNA-seq profiling a molecular signature of Hepatocellular Carcinoma samples that correlates with survival. The samples were retrospectively derived from hepatocellular carcinoma tissue as well as non-tumor tissue from the livers of the same patients. The bioinformatical analysis of 32 pairs RNA-seq datasets were obtained from human RNAs on Illumina Hiseq-PE150. Due to the lack of biological sample duplication, this datasets were used hisat2 2.1.0 and gfold v1.1.4 for expression analysis to identify differences in gene expression between tumors and adjacent tissues. (including up- and down-regulation).

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d5080ccf-6024-42b1-ae2f-e1770fa19cf9 - samples

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.

| EGAD00001010194 | EGA

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