Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA274696 | ENA |
REPOSITORIES: ENA
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Project description:Our results indicate that oxidation of TAF10 by LOXL2 induces its release from its promoters, leading to a block in TFIID-dependent gene transcription. Since TFIID complex is crucial for the expression of Nanog, Klf4, Sox2 and Oct4 and for maintaining the pluripotent state of embryonic stem cells, TAF10 oxidation by LOXL2 leads to inactivation of the pluripotency genes and a loss of pluripotent capacity in embryonic stem cells. Moreover, in vivo results demonstrate an essential role of LOXL2 in neural differentiation during zebrafish development: in the absence of LOXL2 the neural progenitor gene Sox2 is aberrantly overexpressed and neural differentiation is impaired. 12 samples were analyzed: mES transduced with control shRNA (n=3); mES transduced with LOXL2 shRNA (n=3), ES transduced with control shRNA and treated with RA (n=3); ES transduced with LOXL2 shRNA and treated with RA (n=3)
2015-12-21 | E-GEOD-65675 | biostudies-arrayexpress
Project description:SIRT1 deficiency enhances RA induced mESC differentiation
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Project description:Retinoic acid (RA) induction time-course to profile gene expression during mES cell differentiation.
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Project description:Retinoic acid (RA) induction time-course to profile gene expression during mES cell differentiation
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Project description:Chromatin modifications have been implicated in the self-renewal and differentiation of embryonic stem cells (ESCs). However, the function of histone variant H2A.Z in ESCs remains unclear. We show that H2A.Z is highly enriched at promoters and enhancers and is required for both efficient self-renewal and differentiation of murine ESCs. H2A.Z deposition leads to an abnormal nucleosome structure, decreased nucleosome occupancy and increased chromatin accessibility. In self-renewing ESCs, knockdown of H2A.Z compromises OCT4 binding to its target genes and leads to decreased binding of MLL complexes to active genes and of PRC2 complex to repressed genes in self-renewal of ESCs. During differentiation of ESCs, inhibition of H2A.Z also compromises RA-induced RARα binding, activation of differentiation markers and the repression of pluripotency genes. We propose that H2A.Z mediates such contrasting activities by acting as a 'general facilitator' that generates access for a variety of complexes both activating and repressive. ChIP-Seq in murine embryonic stem (mES) cells for H2A.Z and acetylated H2A.Z. ChIP-Seq of H3K4me3, H3K27me3, RbBP5, SUZ12 and OCT4 for mES cells of both H2A.Z RNAi knockdown and shLuc control. ChIP-Seq of RARalpha in H2A.Z knockdown (withdraw of LIF and exposure to RA for 3h) and control cells. MNase-Seq and chromatin accessibility assay using Benzonase digestion followed by next-generation sequencing for mES cells of both H2A.Z RNAi knockdown and shLuc control. ChIP-Seq of H2A.Z and H3K4me3 for mES cells of both MLL4 RNAi knockdown and shLuc control. RNA-Seq for mES cells of H2A.Z knockdown and shluc control. RNA-Seq for embryonic bodies derived from mES cells (H2A.Z knockdown and shLuc control) at day 3 and day 7.
2012-12-20 | E-GEOD-34483 | biostudies-arrayexpress
Project description:Epiblast cells ingress into the primitive streak, undergoing mesendoderm (MES) specification, which subsequently gives rise to the mesoderm and endoderm. Although recent advances in human organoid technology facilitating the study of early post-implantation development, robust human models that accurately recapitulate MES specification and primitive streak (PS) formation remain lacking. Here, we showed that human induced pluripotent stem cells (iPSCs) can be employed to generate three-dimensional (3D) MES organoids that closely mimic in vivo human MES specification, particularly the cells from the anterior region of primitive streak. We revealed that formation of MES organoids depended on the appearance of PTEN, and PTEN abrogation potently impaired the MES organoids-derived definitive endoderm and mesoderm specification. To elucidate the molecular mechanisms underlying the defects induced by PTEN loss, we performed integrative multi-omic analyses‒including RNA sequencing (RNA-seq), assay for transposase-accessible chromatin using sequencing (ATAC-seq), and phospho‒proteomics‒on WT and PTEN−/− MES cells. These analyses indicated retinoic acid (RA) signalling as a critical pathway suppressed by PTEN during MES lineage specification. Moreover, we identified CYP26A1, a RA-degrading enzyme, as a key downstream effector of PTEN in MES cell generation. Notably, our results demonstrated that excessive RA was detrimental, while an optimal level of RA was indispensable for MES cell generation. Overall, our MES organoids provide a valuable platform for investigating human MES specification, and our findings demonstrated PTEN as a driver of MES lineage commitment through the inhibition of RA signalling.
2026-08-19 | GSE301161 | GEO
Project description:tRNA-derived small RNAs in RA induced embryonic stem cell differentiation
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Project description:To characterize the genetic basis of hybrid male sterility in detail, we used a systems genetics approach, integrating mapping of gene expression traits with sterility phenotypes and QTL. We measured genome-wide testis expression in 305 male F2s from a cross between wild-derived inbred strains of M. musculus musculus and M. m. domesticus. We identified several thousand cis- and trans-acting QTL contributing to expression variation (eQTL). Many trans eQTL cluster into eleven ‘hotspots,’ seven of which co-localize with QTL for sterility phenotypes identified in the cross. The number and clustering of trans eQTL - but not cis eQTL - were substantially lower when mapping was restricted to a ‘fertile’ subset of mice, providing evidence that trans eQTL hotspots are related to sterility. Functional annotation of transcripts with eQTL provides insights into the biological processes disrupted by sterility loci and guides prioritization of candidate genes. Using a conditional mapping approach, we identified eQTL dependent on interactions between loci, revealing a complex system of epistasis. Our results illuminate established patterns, including the role of the X chromosome in hybrid sterility.
2014-05-01 | GSE54089 | GEO