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Single-cell RNA-seq reveals cell type-specific transcriptional signatures at the maternal–foetal interface during pregnancy
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Single-cell RNA-seq reveals cell type-specific transcriptional signatures at the maternal–foetal interface during pregnancy
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Journal Article
Single-cell RNA-seq reveals cell type-specific transcriptional signatures at the maternal–foetal interface during pregnancy
2016
Overview
Growth and survival of the mammalian embryo within the uterine environment depends on the placenta, a highly complex vascularized organ comprised of both maternal and foetal tissues. Recent experiments demonstrate that the zinc finger transcriptional repressor
Prdm1
/Blimp1 is essential for specification of spiral artery trophoblast giant cells (SpA-TGCs) that invade and remodel maternal blood vessels. To learn more about functional contributions made by Blimp1+ cell lineages here we perform the first single-cell RNA-seq analysis of the placenta. Cell types of both foetal and maternal origin are profiled. Comparisons with microarray datasets from mutant placenta and
in vitro
differentiated trophoblast stem cells allow us to identify Blimp1-dependent transcripts enriched in SpA-TGCs. Our experiments provide new insights into the functionally distinct cell types present at the maternal–foetal interface and advance our knowledge of dynamic gene expression patterns controlling placental morphogenesis and vascular mimicry.
The zinc finger transcriptional repressor
Prdm1
/Blimp1 is essential for remodelling maternal blood vessels in a subset of trophoblast cells. Here, the authors perform single-cell RNA-seq analysis on this Blimp1+ lineage, identifying functionally distinct cell types present at the maternal–foetal interface.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/100
/ 13/31
/ 38
/ 38/39
/ 38/91
/ 631/136
/ 631/80
/ Animals
/ Cells
/ Embryos
/ Female
/ Gene Expression Regulation, Developmental
/ Humanities and Social Sciences
/ Placenta
/ Positive Regulatory Domain I-Binding Factor 1 - genetics
/ Positive Regulatory Domain I-Binding Factor 1 - metabolism
/ Science
