Sirtuin-1 is required for proper trophoblast differentiation and placental development
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE100279 | GEO | 2018/01/24
REPOSITORIES: GEO
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Project description:Robust identification of placental PPARg target genes via mutliple PPARg-dependence criteria. Integration of differential expression data from Pparg-null, Rxra-null, Med1-nul and Ncoa6-null placentas and from WT and Pparg-null Trophoblast stem cells (TSC) differentiated for 2 or 4 days in the presence or absence of the PPARg agonist Rosiglitazone (Rosi). [Placentas] Three pools of three WT placentas, each vs a litter-matched pool of three Pparg-null placentas Three pools of three WT placentas, each vs a litter-matched pool of three Rxra-null placentas Three pools of three WT placentas, each vs a litter-matched pool of three Med1-null placentas Three pools of three WT placentas, each vs a litter-matched pool of three Ncoa6-null placentas [Trophoblast stem cells (TSC)] Three independent WT TSC lines differentiated for two and four days in the presence or absence of Rosi vs two independent Pparg-null TSC lines differntiated for the same durations in the presence of Rosi
2012-07-09 | E-GEOD-39233 | biostudies-arrayexpress
Project description:Robust identification of placental PPARg target genes via mutliple PPARg-dependence criteria. Integration of differential expression data from Pparg-null, Rxra-null, Med1-nul and Ncoa6-null placentas and from WT and Pparg-null Trophoblast stem cells (TSC) differentiated for 2 or 4 days in the presence or absence of the PPARg agonist Rosiglitazone (Rosi).
2012-07-10 | GSE39233 | GEO
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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.
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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.
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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.
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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.
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2024-11-21 | E-MTAB-12463 | biostudies-arrayexpress
Project description:Elf5 is a transcription factor with pivotal roles in the trophoblast compartment where it reinforces a trophoblast stem cell (TSC)-specific transcriptional circuit. However, Elf5 is also present in differentiating trophoblast cells that have ceased to express other TSC genes such as Cdx2 and Eomes. In the current study we aimed to elucidate the context-dependent role of Elf5 at the interface between TSC self-renewal and onset of differentiation. We demonstrate that precise levels of Elf5 are critical for normal expansion of the TSC compartment and embryonic survival, as Elf5 overexpression triggers precocious trophoblast differentiation. Through integration of protein interactome, transcriptome and genome-wide chromatin immunoprecipitation data we reveal that this abundance-dependent function is mediated through a shift in preferred Elf5 binding partners; in TSCs, Elf5 interaction with Eomes recruits Tfap2c to triply occupied sites at TSC-specific genes driving their expression. By contrast, the Elf5 and Tfap2c interaction becomes predominant as their protein levels increase. This triggers binding to double and single occupancy sites that harbour the cognate Tfap2c motif, causing activation of the associated differentiation-promoting genes. These data place Elf5 at the centre of a stoichiometry-sensitive transcriptional network where it acts as molecular switch governing the balance between TSC proliferation and differentiation.
2015-12-01 | PXD003145 | Pride