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A new female embryonic stem cell system reveals the requirement to open promoter chromatin to establish X chromosome inactivation.

ABSTRACT: A new female embryonic stem cell system reveals the requirement to open promoter chromatin to establish X chromosome inactivation.

PROVIDER: PRJNA564676 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10090600.fastq.gz	Fastqsanger.gz
	SRR10090601.fastq.gz	Fastqsanger.gz
	SRR10090602.fastq.gz	Fastqsanger.gz
	SRR10090603.fastq.gz	Fastqsanger.gz
	SRR10090604.fastq.gz	Fastqsanger.gz

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A new female embryonic stem cell system reveals the requirement to open promoter chromatin to establish X chromosome inactivation.

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Project description:During meiotic prophase in male mammals, the heterologous X and Y chromosomes remain largely unsynapsed, and meiotic sex chromosome inactivation (MSCI) leads to formation of the transcriptionally silenced XY body. In birds, the heterogametic sex is female, carrying Z and W chromosomes (ZW), whereas males have the homogametic ZZ constitution. During chicken oogenesis, the heterologous ZW pair reaches a state of complete heterologous synapsis, and this might enable maintenance of transcription of Z- and W chromosomal genes during meiotic prophase. Herein, we show that the ZW pair is transiently silenced, from early pachytene to early diplotene using immunocytochemistry and gene expression analyses. We propose that ZW inactivation is most likely achieved via spreading of heterochromatin from the W on the Z chromosome. Also, persistent meiotic DNA double-strand breaks (DSBs) may contribute to silencing of Z. Surprisingly, gammaH2AX, a marker of DSBs, and also the earliest histone modification that is associated with XY body formation in mammalian and marsupial spermatocytes, does not cover the ZW during the synapsed stage. However, when the ZW pair starts to desynapse, a second wave of gammaH2AX accumulates on the unsynapsed regions of Z, which also show a reappearance of the DSB repair protein RAD51. This indicates that repair of meiotic DSBs on the heterologous part of Z is postponed until late pachytene/diplotene, possibly to avoid recombination with regions on the heterologously synapsed W chromosome. Two days after entering diplotene, the Z looses gammaH2AX and shows reactivation. This is the first report of meiotic sex chromosome inactivation in a species with female heterogamety, providing evidence that this mechanism is not specific to spermatogenesis. It also indicates the presence of an evolutionary force that drives meiotic sex chromosome inactivation independent of the final achievement of synapsis.

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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.

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Project description:Imprinted X-inactivation is a paradigm of mammalian transgenerational epigenetic regulation resulting in silencing of genes on the paternally inherited X-chromosome. The preprogrammed fate of the X-chromosomes is thought to be controlled in cis by the parent-of-origin-specific expression of two opposing long non-coding RNAs, Tsix and Xist, in mice. Exclusive expression of Tsix from the maternal-X has implicated it as the instrument through which the maternal germline prevents inactivation of the maternal-X in the offspring. Here, we show that Tsix is dispensable for inhibiting Xist and X-inactivation in the early embryo and in cultured stem cells of extra-embryonic lineages. Tsix is instead required to prevent Xist expression as trophectodermal progenitor cells differentiate. Despite induction of wild-type Xist RNA and accumulation of histone H3-K27me3, many Tsix-mutant X-chromosomes fail to undergo ectopic X-inactivation. We propose a novel model of lncRNA function in imprinted X-inactivation that may also apply to other genomically imprinted loci.

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Project description:To investigate the interplay of X-chromosome status and meiosis during primordial germ cell (PGC) maturation, we differentiated mouse embryonic stem cells (ESCs) via epiblast-like cells (EpiLCs) into primordial germ cell like cells (PGCLCs) and further into meiotic germ cells. During the differentiation of PGCLCs, we assessed the kinetics of X-chromosome inactivation and reactivation. We generated allele-specific total RNA-seq datasets to assess gene inactivation and reactivation dynamics, as well as allele-specific single-cell RNA-seq using SMART-Seq v5 to investigate the interplay of meiosis and X-chromosome status in germ cells.

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Achieving Stable X-chromosome Inactivation in Human Embryonic Stem Cells

Project description:X-inactivation is a paradigm of epigenetic transcriptional regulation. Human embryonic stem cells (hESCs) that harbor an inactivated X-chromosome often undergo erosion of X-inactivation upon prolonged culture. Here, we investigate the sources of X-inactivation instability by deriving new primed pluripotent hESC lines. We find that the composition of culture media dramatically influenced the expression of XIST lncRNA, a key regulator of X-inactivation. hESCs cultured in a defined medium stably maintained XIST RNA coating, whereas hESCs cultured in the widely-used mTeSR1 medium lost XIST RNA expression. We pinpointed lithium chloride in mTeSR1 as a cause of XIST RNA loss. The addition of LiCl or inhibitors of glycogen synthase kinase 3 (GSK-3) proteins, which are inhibited by lithium, to the defined hESC culture medium impeded XIST expression. Together, these data may reconcile the observed variations in X-inactivation in hESCs and inform the culture of pluripotent stem cells for disease modeling and regenerative medicine.

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