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An epigenetic timer of gestation length in mice [CUT&RUN]

ABSTRACT: An epigenetic timer of gestation length in mice [CUT&RUN]

PROVIDER: PRJNA1015689 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26044900_1.fastq.gz	Fastqsanger.gz
	SRR26044900_2.fastq.gz	Fastqsanger.gz
	SRR26044901_1.fastq.gz	Fastqsanger.gz
	SRR26044901_2.fastq.gz	Fastqsanger.gz
	SRR26044902_1.fastq.gz	Fastqsanger.gz

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An epigenetic timer of gestation length in mice [scRNA-Seq]

Project description:Timing mechanisms in biology remain poorly understood. As one prime example, little is known about the mechanisms that specify how long the gestating uterus will remain quiescent before entering labor1. Our lack of insight into this fundamental question, which applies to all mammalian species, also limits investigation into potential causes of preterm labor, a major human pregnancy complication. Here, we provide evidence that gestation length in mice is determined by an epigenetic timer that runs autonomously within the fibroblasts of the pregnant uterus. The timer is set during the peri-implantation period when select genomic loci establish appropriate levels of the repressive histone mark H3K27me3. These loci then progressively lose H3K27me3, thereby scheduling the uterine cell state transitions and associated gene expression changes of late gestation that are the proximal mediators of labor onset. Overwinding of the timer’s peri-implantation setpoint via genetic ablation of the histone demethylase KDM6B delays these transitions and extends gestation length. These results provide insight into how complex tissues employ epigenetic pathways to specify the timing of discrete biological events. We also anticipate that further dissection of the ways such uterine programming controls gestation length may suggest novel approaches for improving human pregnancy outcomes.

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An epigenetic timer of gestation length in mice [scRNA-Seq]

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An epigenetic timer of gestation length in mice [CUT&RUN]

Project description:Current efforts investigating parturition timing mechanisms have focused on the proximal triggers of labor onset generated in late gestation. By studying the delayed parturition phenotype of mice with uterine fibroblast deficiencies in the histone H3K37me3 demethylase KDM6B, we provide evidence that parturition timing is regulated by events that take place in early pregnancy. Immediately after copulation, uterine fibroblasts engage in a locus-specific, epigenetic program that abruptly adjusts H3K27me3 levels across their genome. In the absence of KDM6B, many of the adjusted loci over-accumulate H3K27me3. This over-accumulation leads to nearby genes being misexpressed in mid-to-late gestation, a delayed effect partly attributable to a second locus-specific but KDM6B-independent process initiated within uterine fibroblasts soon after implantation. This second process employs progressive H3K27me3 loss to temporally structure post-midgestational patterns of gene induction. Further dissection of the ways uterine programming controls parturition timing may have relevance to human pregnancy complications such as preterm labor.

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G1 length dictates heterochromatin landscape [CUT&RUN]

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