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Next generation sequencing in SETD5-depleted Huh7 cells.

ABSTRACT: To analyze transcriptomic changes in SETD5-deficient Huh7 cells, we performed RNA-sequencing.

ORGANISM(S): Homo sapiens

PROVIDER: GSE193431 | GEO | 2022/09/15

REPOSITORIES: GEO

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Next Generation Sequencing Facilitates Quantitative Analysis of ISL1 Regulated Transcriptomes

Project description:The goals of this study are to analyze the transcriptome profiling (RNA-seq) after ISL1 overexpression in Huh7 cells.

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Next Generation Sequencing Analysis of control and SRSF2-/- Huh7 cells Transcriptomes

Project description:We generated the SRSF2-/- Huh7 cells,and collected the cells at 2 days after transfected with siRNA. Then, we extracted RNAs and performed next generation sequencing. By comparing sequencing data from control and SRSF2 -/- samples, we profiled the alternative splicing events and gene expression regulated by SRSF2 in HCC.

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Transcriptional profiling of Setd5 heterozygous and knockout mouse embryonic stem cells

Project description:SET-domain containing proteins play a vital role in regulating gene expression during development through modifications in chromatin structure. To study molecular function of SET domain containing 5 (Setd5), we assessed global changes in the mouse embryonic stem cell transcriptome when Setd5 gene is knocked out.

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Next generation sequencing analysis of epididymal adipose tissue (II)

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Expression data from SETD5-expressing 3T3-L1 cells.

Project description:SETD5 target genes in 3T3-L1 cells were analyzed.

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SETD5 haploinsufficiency affects mitochondrial compartment in neural cells

Project description:Neurodevelopmental disorders (NDDs) are heterogeneous conditions due to alterations of a variety of molecular mechanisms and cell dysfunctions. Epigenetic basis of NDDs have been reported in an increasingly number of cases while mitochondrial dysfunctions are more common within NDD patients than in the general population. Here, we investigated experimental models of Setd5 haploinsufficiency, that leads to NDDs in humans due to chromatin defects, and uncovered that mitochondrial dysfunction participates in the pathogenesis. Mitochondrial impairment is facilitated by transcriptional aberrations that follow the decrease of SETD5 enzyme. Low levels of SETD5 resulted in fragmented mitochondria, less mitochondrial potential and ATP production both in neural precursors and neurons. Mitochondria were miss-localized in mutant neurons, with few organelles within neurites and synapses. Our study explores the epigenetics/mitochondria interplay as an important aspect of NDD pathophysiology and defines the impairments of mitochondrial functionality and dynamics as new therapeutic targets for disorders associated with loss of SETD5.

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SETD5 regulates the OGT-catalyzed O-GlcNAcylation of RNA polymerase II, which is involved in the stemness of colorectal cancer cells

Project description:The dosage-dependent recruitment of RNA polymerase II (Pol II) at the promoters of genes related to neurodevelopment and stem cell maintenance is required for transcription by the fine-tuned expression of SET-domain-containing protein 5 (SETD5). Pol II O-GlcNAcylation by O-GlcNAc transferase (OGT) is critical for preinitiation complex formation and transcription cycling. SETD5 dysregulation has been linked to stem cell-like properties in some cancer types; however, the role of SETD5 in cancer cell stemness has not yet been determined. We here show that aberrant SETD5 overexpression induces stemness in colorectal cancer (CRC) cells. SETD5 overexpression causes the upregulation of PI3K-AKT pathway-related genes and cancer stem cell (CSC) markers such as CD133, Kruppel-like factor 4 (KLF4), and estrogen-related receptor beta (ESRRB), leading to the gain of stem cell-like phenotypes. Our findings also revealed a functional relationship between SETD5, OGT, and Pol II. OGT-catalyzed Pol II glycosylation depends on SETD5, and the SETD5-Pol II interaction weakens in OGT-depleted cells, suggesting a SETD5-OGT-Pol II interdependence. SETD5 deficiency reduces Pol II occupancy at PI3K-AKT pathway-related genes and CD133 promoters, suggesting a role for SETD5-mediated Pol II recruitment in gene regulation. Moreover, the SETD5 depletion nullified the SETD5-induced stemness of CRC cells and Pol II O-GlcNAcylation. These findings support the hypothesis that SETD5 mediates OGT-catalyzed O-GlcNAcylation of RNA Pol II, which is involved in cancer cell stemness gain via CSC marker gene upregulation.

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ChIP-sequence analysis of H3K27ac, H3K4me1, and SETD5 in 3T3-L1 preadipocytes.

Project description:Enhancer activation is essential for cell-type specific gene expression during cellular differentiation, however, how enhancers transition from a hypoacetylated “primed” state to a hyperacetylated-active state is incompletely understood. Here, we show SET domain-containing 5 (SETD5) forms a complex with NCoR-HDAC3 co-repressor that prevents histone acetylation of enhancers for two master adipogenic regulatory genes Cebpa and Pparg early during adipogenesis. The loss of SETD5 from the complex is followed by enhancer hyperacetylation. SETD5 protein levels were transiently increased and rapidly degraded prior to enhancer activation providing a mechanism for the loss of SETD5 during the transition. We show that induction of the CDC20 co-activator of the ubiquitin ligase leads to APC/C mediated degradation of SETD5 during the transition and this operates as a molecular switch that facilitates adipogenesis.

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