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Resf1 is required for normal placental development and configuration of trophoblast cell-specific heterochromatin [RNA-seq]

ABSTRACT: Resf1 (Retroelement silencing factor 1) is involved in retroelement silencing cooperated with H3K9 methyltransferase SETDB1 by regulating H3K9 methylation in mouse embryonic stem cells (mESCs). However, it remains unknown whether Resf1 functions in retroelement silencing in vivo, and has a role in development. To address this question, we established Resf1-deficient mice. The Resf1-deficient mice show developmental delay, partial embryonic lethality, and placental abnormalities. Remarkably, retroelements are also upregulated in the Resf1-deficient placenta, and this upregulation of retroelements correlates with elevated expression of nearby genes. Additionally, to determine whether Resf1 functions within the trophoblast lineage—given the heterogeneous cellular composition of the placenta—we established Resf1-deficient trophoblast stem cell (TSC) lines. Both undifferentiated TSCs and differentiated TSCs (D-TSCs) display increased retroelement expression along with elevated levels of genes associated with placental development. Furthermore, Resf1-deficient TSCs exhibit compromised maintenance of H3K9me3 domains, leading to instability. In summary, our findings illuminate Resf1's multifaceted roles beyond retroelement silencing, uncovering its significance in developmental processes and its intricate involvement in trophoblast lineage regulation.

ORGANISM(S): Mus musculus

PROVIDER: GSE308515 | GEO | 2026/05/21

REPOSITORIES: GEO

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Resf1 is required for normal placental development and configuration of trophoblast cell-specific heterochromatin

Project description:Resf1 (Retroelement silencing factor 1) is involved in retroelement silencing cooperated with H3K9 methyltransferase SETDB1 by regulating H3K9 methylation in mouse embryonic stem cells (mESCs). However, it remains unknown whether Resf1 functions in retroelement silencing in vivo, and has a role in development. To address this question, we established Resf1-deficient mice. The Resf1-deficient mice show developmental delay, partial embryonic lethality, and placental abnormalities. Remarkably, retroelements are also upregulated in the Resf1-deficient placenta, and this upregulation of retroelements correlates with elevated expression of nearby genes. Additionally, to determine whether Resf1 functions within the trophoblast lineage—given the heterogeneous cellular composition of the placenta—we established Resf1-deficient trophoblast stem cell (TSC) lines. Both undifferentiated TSCs and differentiated TSCs (D-TSCs) display increased retroelement expression along with elevated levels of genes associated with placental development. Furthermore, Resf1-deficient TSCs exhibit compromised maintenance of H3K9me3 domains, leading to instability. In summary, our findings illuminate Resf1's multifaceted roles beyond retroelement silencing, uncovering its significance in developmental processes and its intricate involvement in trophoblast lineage regulation.

2026-05-21 | GSE326675 | GEO

Resf1 is required for normal placental development and configuration of trophoblast cell-specific heterochromatin [ChIP-seq]

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The Gag Protein PEG10 Binds to RNA and Regulates Trophoblast Stem Cell Lineage Specification

Project description:Peg10 (paternally expressed gene 10) is an imprinted gene that is essential for placental development (1). It is thought to derive from a Ty3-gyspy LTR (long terminal repeat) retrotransposon and retains Gag and Pol-like domains (2). Here we show that the Gag domain of PEG10 can promote vesicle budding similar to the HIV p24 Gag protein. Expressed in a subset of mouse endocrine organs in addition to the placenta, PEG10 was identified as a substrate of the deubiquitinating enzyme USP9X. Consistent with PEG10 having a critical role in placental development, PEG10-deficient trophoblast stem cells (TSCs) exhibited impaired differentiation into placental lineages. PEG10 expressed in wild-type, differentiating TSCs was bound to many cellular RNAs including Hbegf (Heparin-binding EGF-like growth factor), which is known to play an important role in placentation (3). Expression of Hbegf was reduced in PEG10-deficient TSCs suggesting that PEG10 might bind to and stabilize RNAs that are critical for normal placental development.

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The Fgf/Erf/NCoR1/2 repressive axis controls trophoblast cell fate

Project description:Here, we demonstrate that upon inhibition of the Fgf/Erk pathway in mouse trophoblast stem cells (TSCs), the Ets2 repressor factor (Erf) interacts with components of the Nuclear Receptor Corepressor Complex 1 and 2 (NCoR1 and NCoR2). Upon attenuation of Fgf signalling, unphosphorylated, nuclear Erf recruits the NCoR1/2 complex to key trophoblast genes, brings about their transcriptional silencing and facilitates differentiation and placental development.

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Unraveling the role of TCF7L2 in self-renewal and differentiation of trophoblast stem cells (TSCs) [RNA-Seq]

Project description:Extravillous trophoblasts (EVTs) are essential for placental development, anchoring the placenta, invading the maternal decidua, and remodeling spiral arteries. TCF7L2, expressed in human placental tissues and EVTs, controls EVT motility. However, its targets and role in early trophoblast differentiation are not well understood. Using trophoblast stem cells (TSCs) as model system, we investigated roles of TCF7L2 in self-renewal and differentiation of trophoblasts using RNA-seq and ChIP-seq.

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Chromosomal instability in human trophoblast stem cells and placenta

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Project description:Placental infection plays a central role in the pathogenesis of congenital human cytomegalovirus (HCMV) infections and is a cause of fetal growth restriction and pregnancy loss. HCMV can replicate in some trophoblast cell types, but it remains unclear how the virus evades antiviral immunity in the placenta and how infection compromises placental development and function. Human trophoblast stem cells (TSCs) can be differentiated into extravillous trophoblasts (EVTs) and syncytiotrophoblasts (STBs). This study assessed the utility of TSCs as a model of HCMV infection in the first trimester placenta. TSCs and TSC-derived EVTs and STBs were infected with HCMV (TB40/Ewt-mCherry). RNA was isolated from infected cells at 24, 48, and 72 hours post-infection and Illumina RNA-Sequencing was used to measure viral and host gene expression. Viral gene expression in TSCs does not follow the kinetic patterns observed during lytic infection in fibroblasts. Canonical antiviral responses were largely not observed in HCMV-infected TSCs and TSC-derived trophoblasts. Rather, infection dysregulated factors involved in cell identity, differentiation, and WNT signaling.

2023-12-14 | GSE248772 | GEO

Induction of human trophoblast stem-like cells from primed pluripotent stem cells

Project description:The placenta is a transient but important multifunctional organ crucial for healthy pregnancy for both mother and fetus. Nevertheless, limited access to human placenta samples and the paucity of a proper in vitro model system has hampered our understanding of the mechanisms underlying early human placental development and placenta-associated pregnancy complications. To overcome these constraints, we established a simple procedure with a short-term treatment of bone morphogenetic protein 4 (BMP4) in trophoblast stem cell culture medium (TSCM) to convert human primed pluripotent stem cells (PSCs) to trophoblast stem-like cells (TSLCs). These TSLCs show not only comparable morphology and gene expression profile to bona fide human trophoblast stem cells (TSCs) but also long-term self-renewal capacity with bipotency that allows the cells to differentiate into extravillous trophoblasts (EVT) and syncytiotrophoblasts (ST). These indicate that TSLCs are equivalent to genuine human TSCs. Our data suggest a straightforward approach to make human TSCs directly from pre-existing primed PSCs and provide a valuable opportunity to study human placenta development and pathology even from patients with placenta-related diseases.

2021-12-31 | GSE178162 | GEO

Lsd1 coordinates trophoblast development by retaining stem cells in their niche and directing cell fate

Project description:Stem cells reside in specific niches providing stemness-maintaining environments. Thus, the regulated migration from these niches is associated with differentiation onset. However, mechanisms retaining stem cells in their niche remain poorly understood. Here, we show that the epigenetic regulator lysine-specific demethylase 1 (Lsd1) organises the trophoblast niche of the early mouse embryo by coordinating migration and invasion of trophoblast stem cells (TSCs). Lsd1 deficiency leads to the depletion of the stem cell pool resulting from precocious migration of TSCs. Migration is induced by premature expression of the transcription factor Ovol2 that is repressed by Lsd1 in undifferentiated wild-type TSCs. Increasing Ovol2 levels suffices to recapitulate the migration phenotype. Furthermore, Lsd1-deficient TSCs exhibit a developmental bias towards cells of the syncytiotrophoblast and impaired spongiotrophoblast and trophoblast giant cell differentiation. In summary, we describe that the epigenetic modifier Lsd1 coordinates placental development by retaining TSCs in their niche and directing trophoblast differentiation. Mouse trophoblast stem cells (TSCs) were isoloated from a single conditional Lsd1-deficient mouse (Lsd1tm1SchM-CM-<le). Deletion of Lsd1 was induced eight days before the collection of RNA by addition of 0.2 M-BM-5M 4OH-tamoxife. Cells were isolated at successive stages of differentiation for total RNA extraction and hybridization on Affymetrix microarrays. To that end, we harvested cells at three time-points: before induction of differentiation (d0), two days after induction of differentiation (d2), and four days after induction of differentiation (d4). Three replicates (1, 2, 3) for control (-) and Lsd1-deficeint (+) cells were included for each differentiation stage.

2014-01-17 | E-GEOD-38277 | biostudies-arrayexpress

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