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Modulation of gene expression by ZNF143, THAP11 and NOTCH1 via overlapping binding sites in mammalian cells

ABSTRACT: In this study we investigated the genome wide DNA binding profile of ZNF143 and ICN1 in human and murine cells. We also analyzed the expression profile in human cells after overexpression or knockdown of ZNF143.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE39263 | GEO | 2013/02/13

SECONDARY ACCESSION(S): PRJNA170436

REPOSITORIES: GEO

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Modulation of gene expression by ZNF143, THAP11 and NOTCH1 via overlapping binding sites in mammalian cells

Project description:In this study we investigated the genome wide DNA binding profile of ZNF143 and ICN1 in human and murine cells. We also analyzed the expression profile in human cells after overexpression or knockdown of ZNF143. To identify ZNF143 targets we performed ChIP-seq on 4 human cells lines and 3 murine cell types. We also identified, by ChIP-seq, ICN1 binding sites in HPB-ALL cells. To identify directly regulated genes by ZNF143, we analyzed, by RNA-seq, the expression profile after knockdown and overexpression of the transcription factor.

2013-02-13 | E-GEOD-39263 | biostudies-arrayexpress

Modulation of gene expression via overlapping binding sites exerted by ZNF143, Notch1 and THAP11.

Project description:ZNF143 is a zinc-finger protein involved in the transcriptional regulation of both coding and non-coding genes from polymerase II and III promoters. Our study deciphers the genome-wide regulatory role of ZNF143 in relation with the two previously unrelated transcription factors Notch1/ICN1 and thanatos-associated protein 11 (THAP11) in several human and murine cells. We show that two distinct motifs, SBS1 and SBS2, are associated to ZNF143-binding events in promoters of >3000 genes. Without co-occupation, these sites are also bound by Notch1/ICN1 in T-lymphoblastic leukaemia cells as well as by THAP11, a factor involved in self-renewal of embryonic stem cells. We present evidence that ICN1 binding overlaps with ZNF143 binding events at the SBS1 and SBS2 motifs, whereas the overlap occurs only at SBS2 for THAP11. We demonstrate that the three factors modulate expression of common target genes through the mutually exclusive occupation of overlapping binding sites. The model we propose predicts that the binding competition between the three factors controls biological processes such as rapid cell growth of both neoplastic and stem cells. Overall, our study establishes a novel relationship between ZNF143, THAP11 and ICN1 and reveals important insights into ZNF143-mediated gene regulation.

| S-EPMC3627581 | biostudies-literature

Modulation of gene expression by ZNF143, THAP11 and NOTCH1 via overlapping binding sites in mammalian cells

Project description:Modulation of gene expression by ZNF143, THAP11 and NOTCH1 via overlapping binding sites in mammalian cells

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Znf143 binding sites in U937 cells by ChIPexo

Project description:We performed ChIPexo sequencing to identify the binding sites of Znf143 in the U937 cell line.

2017-01-01 | GSE65130 | GEO

Mapping of Notch1 binding sites in a mouse immature T cell line

2014-04-02 | GSE46114 | GEO

Genomic Determinants of THAP11/ZNF143/HCFC1 Complex Recruitment to Chromatin.

Project description:The THAP11 and ZNF143 transcription factors recognize overlapping DNA sequences and are reported to exhibit signs of both competitive and cooperative binding. HCFC1 serves as a scaffold protein, bridging interactions between transcription factors, including THAP11 and ZNF143, and transcriptional coregulators. The exact mechanism of how DNA sequences guide the recruitment of the THAP11/ZNF143/HCFC1 complex to chromatin is still controversial. In this study, we use chromosomally integrated synthetic constructs and clustered regularly interspaced short palindromic repeat (CRISPR)-Cas9-mediated approaches in intact cells to elucidate the role of the DNA sequence in the recruitment of this complex and to establish its biological relevance. We show that the ACTACA submotif, shared by both THAP11 and ZNF143, directs the recruitment of THAP11 and HCFC1 to ZNF143-occupied loci. Importantly, its position, spacing, and orientation relative to the ZNF143 core motif are critical for this action. CRISPR-Cas9-mediated alterations of the ACTACA submotif at endogenous promoters recapitulated results obtained with synthetic constructs and resulted in altered gene transcription and histone modifications at targeted promoters. Our in vivo approaches provide strong evidence for the molecular role of the ACTACA submotif in THAP11, ZNF143, and HCFC1 cooperative recruitment to chromatin and its biological role in target gene expression.

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Mapping of Notch1 binding sites in a mouse immature T cell line

Project description:We used an immature mouse T cell line engineered to express a biotinylated form of the cleaved form of Notch1 (ICN1). ICN1-bound sites were precipitated with streptavidin-coated beads and subjected to ChIP-sequencing. Beko cells correspond to a spontaneous T lymphoma immature cell line derived from a TCRb deficient mouse. These cells were engineered to express a biotin-tagged-ICN1 and the bacterial biotin ligase BirA (Bio-ICN1) or just BirA as a control (Bio). Chromatin from both cell lines was subjected to strepatavidin-mediated precipitation and subjected to sequencing with the Illumina GAII sequencer as single end 36 base pair reads.

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ZNF143 is a transcriptional regulator of nuclear-encoded mitochondrial genes that acts independently of looping and CTCF

Project description:Gene expression is orchestrated by transcription factors (TFs), which bind to DNA in a sequence-specific manner, and by spatial genome structure, which constrains and shapes TF activity. Zinc finger protein 143 (ZNF143/ZFP143) is a TF that has been implicated in both gene activation and 3D genome organisation. We have generated an acute ZNF143/ZFP143 depletion system to study its direct consequences on chromatin looping and gene transcription. The effects of ZNF143/ZFP143 depletion are inconsistent with it being a looping factor, which we further confirmed by systematic analysis of previous studies. However, degradation of ZNF143/ZFP143 led to the down-regulation of hundreds of its targets, which were found to be enriched in nuclear-encoded mitochondrial genes. By studying the consequences of ZNF143/ZFP143 loss in monoculture and in an in vitro embryonic development model, we establish ZNF143/ZFP143 as a conserved transcriptional regulator of cell proliferation and differentiation by modulating mitochondrial functions.

2024-03-08 | PXD049480 | Pride

ZNF143 deletion alters enhancer/promoter looping and CTCF/cohesin geometry [HiChIP]

Project description:The transcription factor ZNF143 contains seven tandem zinc fingers and is involved in 3D genome construction; however, the mechanism by which ZNF143 functions in chromatin looping remains unclear. Here, we show that ZNF143 directionally recognizes diverse genomic sites and is required for chromatin looping between these sites. In addition, ZNF143 is located between CTCF and cohesin at numerous CTCF sites and ZNF143 removal narrows the space between CTCF and cohesin. Moreover, genetic deletion of ZNF143, in conjunction with acute CTCF depletion, revealed that ZNF143 and CTCF collaborate to regulate higher-order genome organization. Thus, ZNF143 is recruited by CTCF to the CTCF sites to regulate TAD formation and genome compartmentalization whereas directional recognition of DNA motifs directly by ZNF143 itself regulates promoter activity via chromatin looping.

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