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Expression data from Smarcd1 knockdown R1 embryonic stem cells

ABSTRACT: We used microarrays to identify the gene expression changes after Smarcd1 knockdown in ESCs and 4 day RA differentiated ESCs

ORGANISM(S): Mus musculus

PROVIDER: GSE65089 | GEO | 2015/03/01

SECONDARY ACCESSION(S): PRJNA272928

REPOSITORIES: GEO

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Expression data from Smarcd1 knockdown R1 embryonic stem cells

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H2A.Z Facilitates Access of Active and Repressive Complexes to Chromatin in Embryonic Stem Cell Self-renewal and Differentiation

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.

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RNA-seq of SMARCD1 knockdown HL60 leukemic cell line in untreated and vitamin D3 treated condition

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Smarcd1 is a “Goldilocks” metastasis modifier gene

Project description:Breast cancer is the most highly diagnosed cancer worldwide, making up around 12% of all diagnosed cancers in 2020. Mortality caused by breast cancer is largely due to metastasis to distant essential organs, and a lack of metastasis-targeted therapies perpetuates incredibly poor outcomes for late-stage patients. Here we have identified a new class of “Goldilocks” genes for metastasis-targeted therapeutic development, through our focus on meiotic genetics and inherited transcriptional network regulation. Building on previous work identifying the CCR4-NOT RNA deadenylase complex in metastasis, we further demonstrate that RNA binding proteins NANOS1, PUM2, and CPSF4 also regulate metastatic potential. Using cell lines, 3D culture, mouse models, and clinical data, we have identified Smarcd1 mRNA, a key target of all three factors, for which high and low expression is associated with positive clinical outcome, but medium expression significantly reduces probability of survival. Applying the theory of “essential genes” from evolution, we have identified an additional 50 genes that span several cellular processes and must be maintained within a discrete window of expression for metastasis to occur. In the case of Smarcd1, small perturbations in expression level significantly reduced metastasis in laboratory mouse models and altered splicing programs of particular relevance to the ER+HER2 enriched patient subtype. Identification of subtype-specific “Golidlocks” metastasis modifier genes creates a new class of genes and catalogue of potential novel targets that when therapeutically “nudged” in either direction may significantly improve late-stage patient outcomes.

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