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Rif1 functions in complex with PRC1.6 to regulate mouse embryonic stem cells fate potential

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE203306 | GEO | 2022/06/09

REPOSITORIES: GEO

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Rif1 functions in complex with PRC1.6 to regulate mouse embryonic stem cells fate potential [RNA-seq]

Project description:To investigate the cooperative function Rif1 and PRC1.6 complex in the regulation of embryonic development and cell differentiation, we selected embryonic stem cells in which each target gene has been knocked down by shRNA or knocked out conditionally. We then performed gene expression profiling analysis using data obtained from RNA-seq of different samples.

2022-06-10 | GSE203305 | GEO

Rif1 functions in complex with PRC1.6 to regulate mouse embryonic stem cells fate potential [ChIP-seq]

Project description:To investigate if Rif1 depletion compromised the accurate genomic targeting of the PRC1.6 complex, we performed ChIP-seq analyses of Rif1, Pcgf6, RNF2, and the H2AK119ub in the control and Rif1-depleted mESCs.

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Rif1 functions in complex with PRC1.6 to regulate mouse embryonic stem cells fate potential

Project description:Rif1 functions in complex with PRC1.6 to regulate mouse embryonic stem cells fate potential

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Rif1 functions in complex with PRC1.6 to regulate mouse embryonic stem cells fate potential [ChIP-seq]

Project description:Rif1 functions in complex with PRC1.6 to regulate mouse embryonic stem cells fate potential [ChIP-seq]

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Rif1 functions in complex with PRC1.6 to regulate mouse embryonic stem cells fate potential [RNA-seq]

Project description:Rif1 functions in complex with PRC1.6 to regulate mouse embryonic stem cells fate potential [RNA-seq]

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A tight control of Rif1 by Oct4 and Smad3 is critical for mouse embryonic stem cell stability.

Project description:Prolonged culture of embryonic stem cells (ESCs) leads them to adopt embryonal carcinoma cell features, creating enormous dangers for their further application. The mechanism involved in ESC stability has not, however, been extensively studied. We previously reported that SMAD family member 3 (Smad3) has an important role in maintaining mouse ESC stability, as depletion of Smad3 results in cancer cell-like properties in ESCs and Smad3-/- ESCs are prone to grow large, malignant teratomas. To understand how Smad3 contributes to ESC stability, we performed microarray analysis to compare the transcriptome of wild-type and Smad3-/- ESCs. We found that Rif1 (RAP1-associated protein 1), a factor important for genomic stability, is significantly upregulated in Smad3-/- ESCs. The expression level of Rif1 needs to be tightly controlled in ESCs, as a low level of Rif1 is associated with ESC differentiation, but a high level of Rif1 is linked to ESC transformation. In ESCs, Oct4 activates Rif1, whereas Smad3 represses its expression. Oct4 recruits Smad3 to bind to Rif1 promoter, but Smad3 joining facilitates the loading of a polycomb complex that generates a repressive epigenetic modification on Rif1 promoter, and thus maintains the expression of Rif1 at a proper level in ESCs. Interestingly, Rif1 short hairpin RNA (shRNA)-transduced Smad3-/- ESCs showed less malignant properties than the control shRNA-transduced Smad3-/- ESCs, suggesting a critical role of Rif1 in maintaining the stability of ESCs during proliferation.

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Project description:Haploid embryonic stem cells (ESCs) have recently been derived from parthenogenetic mouse embryos and offer new possibilities for genetic screens. The ability of haploid ESCs to give rise to a wide range of differentiated cell types in the embryo and in vitro has been demonstrated. However, it has remained unclear whether haploid ESCs can contribute to the germline. Here, we show that parthenogenetic haploid ESCs at high passage have robust germline competence enabling the production of transgenic mouse strains from genetically modified haploid ESCs. We also show that differentiation of haploid ESCs in the embryo correlates with the gain of a diploid karyotype and that diploidisation is the result of endoreduplication and not cell fusion. By contrast, we find that a haploid karyotype is maintained when differentiation to an extra-embryonic fate is forced by induction of Gata6.

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