Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Female human primordial germ cells display X-chromosome dosage compensation despite the absence of X-inactivation [Female]

ABSTRACT: Female human primordial germ cells display X-chromosome dosage compensation despite the absence of X-inactivation [Female]

PROVIDER: PRJNA600254 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10859003.fastq.gz	Fastqsanger.gz
	SRR10859004.fastq.gz	Fastqsanger.gz
	SRR10859005.fastq.gz	Fastqsanger.gz
	SRR10859006.fastq.gz	Fastqsanger.gz
	SRR10859007.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

Female human primordial germ cells display X-chromosome dosage compensation despite the absence of X-inactivation [Female]

Project description:X chromosome dosage compensation is one of the most important epigenetic events in female mammalian development. Although the mouse has served as the primary model to study how genetic equality is established between male and female mammals, it is now appreciated that these mechanisms are not fully conserved in humans. Using human primordial germ cells (hPGCs) as a model together with single cell RNA-sequencing, in vitro differentiation of hPGC like cells and human embryo attachment culture, we show that X-linked gene expression in female hPGCs is compensated to levels found in female somatic cells though a mechanism related to X chromosome dampening rather than X chromosome inactivation. Loss of dampening and decompensation of both X chromosomes occurs when female hPGCs enter meiosis and is coincident with loss of the long non-coding RNAs XIST and XACT. In contrast, differentiation of male hPGCs results in no change in compensation despite loss of XACT. Taken together, future studies of X-linked gene regulation and function in human germ cell development and fertility must take into account the unique and sexually dimorphic dosage compensation occurring during in the prenatal human germline prior to birth.

2020-10-19 | GSE143380 | GEO

Female human primordial germ cells display X-chromosome dosage compensation despite the absence of X-inactivation [Male]

2020-10-19 | GSE143356 | GEO

Female human primordial germ cells display X-chromosome dosage compensation despite the absence of X-inactivation [Female]

Project description:Female human primordial germ cells display X-chromosome dosage compensation despite the absence of X-inactivation [Female]

| PRJNA600258 | ENA

Female human primordial germ cells display X-chromosome dosage compensation despite the absence of X-inactivation [Male]

Project description:Female human primordial germ cells display X-chromosome dosage compensation despite the absence of X-inactivation [Male]

| PRJNA600212 | ENA

Female human primordial germ cells display X-chromosome dosage compensation despite the absence of X-inactivation.

Project description:X-chromosome dosage compensation in female placental mammals is achieved by X-chromosome inactivation (XCI). Human pre-implantation embryos are an exception, in which dosage compensation occurs by X-chromosome dampening (XCD). Here, we examined whether XCD extends to human prenatal germ cells given their similarities to naive pluripotent cells. We found that female human primordial germ cells (hPGCs) display reduced X-linked gene expression before entering meiosis. Moreover, in hPGCs, both X chromosomes are active and express the long non-coding RNAs X active coating transcript (XACT) and X inactive specific transcript (XIST)-the master regulator of XCI-which are silenced after entry into meiosis. We find that XACT is a hPGC marker, describe XCD associated with XIST expression in hPGCs and suggest that XCD evolved in humans to regulate X-linked genes in pre-implantation embryos and PGCs. Furthermore, we found a unique mechanism of X-chromosome regulation in human primordial oocytes. Therefore, future studies of human germline development must consider the sexually dimorphic X-chromosome dosage compensation mechanisms in the prenatal germline.

| S-EPMC7717582 | biostudies-literature

Female human primordial germ cells display X-chromosome dosage compensation despite the absence of X-inactivation [Female]

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

2020-10-19 | GSE143381 | GEO

Female mice lacking Xist RNA show partial dosage compensation and survive to term

Project description:X chromosome inactivation (XCI) compensates for differences in X-chromosome number between male and female mammals. XCI is orchestrated by Xist RNA, whose expression in early development leads to transcriptional silencing of one X-chromosome in the female. Knockout studies have established a requirement for Xist, with inviability of female embryos that inherit an Xist deletion from the father. Here, we report that female mice lacking Xist RNA can, surprisingly, develop and survive to term. Xist-null females are born at lower frequency and are smaller at birth, but organogenesis is mostly normal. Transcriptomic analysis indicates significant overexpression of hundreds of X-linked genes across multiple tissues. Therefore, Xist-null mice can develop to term in spite of a deficiency of dosage compensation. However, the degree of X-autosomal dosage imbalance was less than anticipated (1.14- to 1.36-fold). Thus, partial dosage compensation can be achieved without Xist, supporting the idea of inherent genome balance. Nevertheless, to date, none of the mutant mice has survived beyond weaning stage. Sudden death is associated with failure of postnatal organ maturation. Our data suggest Xist-independent mechanisms of dosage compensation and demonstrate that small deviations from X-autosomal balance can have profound effects on overall fitness.

2016-08-19 | GSE84665 | GEO

Female mice lacking Xist RNA show partial dosage compensation and survive to term

2016-08-19 | E-GEOD-84665 | biostudies-arrayexpress

The X-chromosome dosage compensation program during the development of cynomolgus monkeys

Project description:X-chromosome dosage compensation ensures balanced gene dosage between the X chromosome and autosomes and between the sexes, involving divergent mechanisms among mammals. We elucidated a distinct mechanism for X-chromosome inactivation (XCI) in cynomolgus monkeys, a model for human development. The trophectoderm and cytotrophoblast acquire XCI around implantation through an active intermediate bearing repressive modifications and compacted structure, whereas the amnion, epiblast, and hypoblast maintain such an intermediate protractedly, attaining XCI by a week after implantation. Males achieve X-chromosome up-regulation (XCU) progressively, whereas females show XCU coincidentally with XCI, both establishing the X:autosome dosage compensation by 1 week after implantation. Conversely, primordial germ cells undergo X-chromosome reactivation by reversing the XCI pathway early during their development. Our findings establish a foundation for clarifying the dosage compensation mechanisms in primates, including humans.

2021-11-19 | GSE151149 | 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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data