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Unique Trophoblast Chromatin Environment Mediated by the PcG Protein SFMBT2 [ChIP-seq]

ABSTRACT: Sfmbt2 is a paternally imprinted gene critical for the establishment and maintenance of trophoblast stem cells in mice (Miri K et al., 2013). Inheritance of a gene trap null allele (Sfmbt2gt/gt) results in embryonic lethality by e12.5 due to reduced numbers in all trophoblast cell types. SFMBT2 is a mammalian Polycomb group protein (PcG) and is assumed to act as a master transcriptional regulator. ChIP-seq was performed against endogenous and FLAG-SFMBT2 in trophoblast stem cells (TSCs) to complement the RNA-seq dataset acquired from extraembryonic tissues of wildtype and Sfmbt2gt/gt mice. We aim to determine the binding profile of SFMBT2 in TSCs and how it contributes to the observed transcriptomic profile.

ORGANISM(S): Mus musculus

PROVIDER: GSE115087 | GEO | 2019/08/18

REPOSITORIES: GEO

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Unique Trophoblast Chromatin Environment Mediated by the PcG Protein SFMBT2 [RNA-seq]

Project description:Sfmbt2 is a paternally imprinted gene critical for the establishment and maintenance of trophoblast stem cells in mice (Miri K et al., 2013). Inheritance of a paternal Sfmbt2 gene trap null allele (Sfmbt2gt/gt) results in embryonic lethality by e12.5 due to reduced numbers in all trophoblast cell types. Of note, SFMBT2 is characterized as a Polycomb group (PcG) protein and is assumed to act as a master transcriptional repressor. Through RNA-seq analysis of extraembryonic tissues acquired from both wild-type and Sfmbt2gt/gt embryos, we aim to elucidate differentially expressed genes critical for the dramatic phenotype observed in mutant embryos.

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Unique Trophoblast Chromatin Environment Mediated by the PcG Protein SFMBT2

Project description:Unique Trophoblast Chromatin Environment Mediated by the PcG Protein SFMBT2

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Unique Trophoblast Chromatin Environment Mediated by the PcG Protein SFMBT2 [ChIP-seq]

Project description:Unique Trophoblast Chromatin Environment Mediated by the PcG Protein SFMBT2 [ChIP-seq]

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Unique Trophoblast Chromatin Environment Mediated by the PcG Protein SFMBT2 [RNA-seq]

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Loss of H3K27me3 imprinting in the Sfmbt2 miRNA cluster causes enlargement of cloned mouse placentas

Project description:Abnormal placentation in cloned animals remains an unsolved problem. We demonstrated the involvement of micro RNAs (miRNAs) in the abnormal enlargement (hyperplasia) of placentas in cloned mice. Using a comparative transcriptome analysis of cloned placentas, we noted the consistent upregulation of clustered miRNAs within Sfmbt2, a paternally expressed imprinted gene. This region was biallelically activated by loss of imprinting (LOI) in cloned placentas. Deletion of the maternal allele of the whole miRNA cluster resulted in the correction of their expression levels and upregulation of their putative target genes with antitumor or apoptotic functions. Consequently, the placental size was reduced to the normal level and histology was ameliorated. In contrast, correcting the expression of the LOI genes (Sfmbt2, Gab1, and Scl38a4) in cloned placentas had no impact on placental size. Thus, we identified that LOI of clustered miRNAs within Sfmbt2 in cloned placentas was the major cause of abnormal placental enlargement.

2020-02-29 | GSE129939 | GEO

Loss of H3K27me3 imprinting in the Sfmbt2 miRNA cluster causes enlargement of cloned mouse placentas

2020-02-29 | GSE129541 | GEO

The PcG gene Sfmbt2 is paternally expressed in extraembryonic tissues.

Project description:Genomic imprinting has dramatic effects on placental development, as has been clearly observed in interspecific hybrid, somatic cell nuclear transfer, and uniparental embryos. In fact, the earliest defects in uniparental embryos are evident first in the extraembryonic trophoblast. We performed a microarray comparison of gynogenetic and androgenetic mouse blastocysts, which are predisposed to placental pathologies, to identify imprinted genes. In addition to identifying a large number of known imprinted genes, we discovered that the Polycomb group (PcG) gene Sfmbt2 is imprinted. Sfmbt2 is expressed preferentially from the paternal allele in early embryos, and in later stage extraembryonic tissues. A CpG island spanning the transcriptional start site is differentially methylated on the maternal allele in e14.5 placenta. Sfmbt2 is located on proximal chromosome 2, in a region known to be imprinted, but for which no genes had been identified until now. This possibly identifies a new imprinted domain within the murine genome. We further demonstrate that murine SFMBT2 protein interacts with the transcription factor YY1, similar to the Drosophila PHO-RC.

| S-EPMC2220043 | biostudies-literature

Unique trophoblast chromatin environment mediated by the PcG protein SFMBT2.

Project description:Stem/progenitor cells are maintained by a chromatin environment, mediated in part by Polycomb group (PcG) proteins, which depress differentiation. The trophoblast-specific PcG protein SFMBT2 is known to be required for maintenance of trophoblast progenitors. Rather than binding to trophoblast-specific genes repressed in TSC, SFMBT2 is concentrated at chromocentres and regions rich in repetitive elements, specifically LINE sequences and major satellites, suggesting that it is involved in higher-order organization of the trophoblast genome. It is also found enriched at a subset of ncRNAs. Comparison of ChIP-seq datasets for other chromatin proteins reveals several stereotypical distribution patterns, suggesting that SFMBT2 interacts with several different types of chromatin complexes specific to the trophoblast lineage.

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The Rodent-Specific MicroRNA Cluster within the Sfmbt2 Gene is Imprinted and Essential for Placental Development [miRNA]

Project description:MicroRNAs (miRNAs) represent small noncoding RNAs that are involved in physiologic and developmental processes by negatively regulating expression of target genes. They exist as individual miRNA genes or as polycistronically transcribed gene clusters. The largest miRNA cluster in mice is located in intron 10 of the Sfmbt2 gene, and contains 72 miRNA precursor sequences within approximately 50 kb. Although this miRNA cluster emerged recently in the rodent genome, probably coincidentally with the acquisition of the imprinted control of Sfmbt2, very little is known about its functions. In this study, we generated mice lacking the entire Sfmbt2 miRNA cluster to elucidate its functions during development. Like the Sfmbt2 gene, the Sfmbt2 miRNAs were expressed in the placenta predominantly from the paternal allele. Loss of the paternal allele resulted in severely impaired development of the spongiotrophoblast layer, which usually comprises about half of the fetal placenta. This phenotype was associated with fetal developmental delay or lethality, leading to significant decreases in the number of fetuses and their weights at term. Microarray analysis identified that at least 30 miRNAs in the cluster were actively transcribed in wild-type placentas. Among the predicted targets of these miRNAs, 132 genes were upregulated in the miRNA-deleted placentas. Some of the genes most significantly upregulated, including Gkn2 and Runx1, are known to inhibit cell proliferation by inducing cell cycle arrest or apoptosis. Thus, the Sfmbt2 miRNAs play essential roles in promoting trophoblastic cell proliferation in the placenta, cooperating with the host gene under the same paternal expression control.

2017-02-01 | GSE82054 | 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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