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Chip-seq analysis of meiotic Cohesin complexes (mei-Cohesins) subunits, CTCF, and BORIS/CTCFL in Macaca fascicularis testis

ABSTRACT: The study involved chromatin IP analyzed by high-throughput sequencing analysis using purifird germ cells from M. fascucularis testis M. fascicularis is a monkey with non-seasonal male germ cells production, and the most popular primate for preclinical animal studies. The goal of the study was to investigate the epigenome of M. fscicularis testis with respect to mei-Cohesin complexes, CTCF and BORIS

ORGANISM(S): Macaca fascicularis

PROVIDER: GSE118006 | GEO | 2022/09/30

REPOSITORIES: GEO

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Chip-seq analysis of meiotic Cohesin (mei-Cohesins) subunit REC8 cleaved by separase (REC8*), and SMC3 in Macaca fascicularis testis

Project description:The study aimed to map epigenomic locations of separase-cleaved REC8 using chromatin IP analyzed by high-throughput sequencing on purified germ cells from M. fascicularis testis

2022-11-07 | GSE201989 | GEO

BORIS/CTCFL epigenetically reprograms clustered CTCF binding sites into alternative transcriptional start sites.

Project description:Pervasive usage of alternative promoters leads to deregulation of gene expression in carcinogenesis and may drive the emergence of new genes in spermatogenesis. However, little is known regarding the mechanisms underpinning the activation of alternative promoters. In our present study, we uncovered a novel mechanism by which alternative cancer-testis-specific transcription is activated from the intergenic and intronic clustered CTCF binding sites, which are transcriptionally inert in normal somatic cells. BORIS/CTCFL, a paralog of CTCF with cancer-testis-specific expression forms a heterodimer with CTCF at the clustered binding sites thus triggering epigenetic reprogramming of these sites into units of active transcription. BORIS binding to CTCF sites leads to the recruitment of chromatin-remodeling factor SRCAP, with subsequent replacement of H2A histone with H2A.Z, therefore creating a more relaxed chromatin state in the nucleosomes flanking the clustered binding sites. This facilitates opening of chromatin beyond CTCF/BORIS binding sites and paves the way to the recruitment of multiple additional transcription factors, thereby activating transcription from a given binding site. We demonstrate that the CTCF binding sites, epigenetically reprogrammed by ectopic BORIS expression can drive the expression of cancer-testis genes, long-noncoding RNAs, retro-pseudogenes, and dormant transposable elements harbored by activated long transcripts. Taking together, our results reveal that BORIS functions as a transcription factor that epigenetically reprograms clustered CTCF binding sites into transcriptional start sites, promoting transcription from alternative promoters in both germ cells and cancer cells.

2024-01-03 | GSE207058 | GEO

Expression profiling of BORIS knockout mice testis

Project description:To identify differentially expressed genes in Boris KO testis, gene expression profilings were performed with NIAID mouse customized arrays. Gene expressions of five biological replicates of Boris KO testis were compared to those of wild type testis. Total RNAs from WT and BORIS KO testes prepared from P14 mice were labelled with Cy5 and Cy3, respectively. Five sets of each genotype were studied.

2010-06-05 | E-GEOD-19162 | biostudies-arrayexpress

Expression profiling of BORIS knockout mice testis

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RNA-seq analysis of BORIS/CTCFL knockdown in K562 cell line

Project description:The study involved transcriptome analysis using RNA-seq knockdown of BORIS/CTCFL gene expression in K652 cancer cell line using inducible shRNA. The K562 cell line is the only cancer cell line that is known to be dependent on BORIS for proliferation and self-renewal of stemness. The goal of the study was to investigate the early/immediate transcriptional response to BORIS downregulation (over 10-fold reduction in protein level) using an inducible shRNA.

2017-09-25 | GSE99825 | GEO

RNA-seq analysis of doxycycline-inducible BORIS/CTCFL expression in the metastatic melanoma cell line MM057

Project description:Brother of Regulator of Imprinted Sites (BORIS) is a DNA binding protein with high similarity to CCCTC binding factor (CTCF), a multifunctional transcription factor that plays an important role in genome organization. Like CTCF, BORIS plays a role in transcriptional regulation. BORIS becomes aberrantly expressed in melanoma with a higher frequency in metastatic tumors compared to primary tumors, which indicates a role for BORIS in melanoma progression. Currently, little is known about the role of BORIS in melanoma. To gain insight into the functional role of BORIS in melanoma we established doxycycline-inducible BORIS expression in the MM057 melanoma cell line that harbors a proliferation-associated transcriptome. Next, we used RNA-seq to investigate BORIS-mediated transcriptional changes. We show that differentially expressed genes are enriched among invasion-related processes and gene signatures, indicating that BORIS expression contributes to an EMT-like switch from a proliferation to invasion-associated transcriptome. In agreement with these findings, we demonstrate that BORIS overexpression leads to reduced proliferation and increased migration and invasion. Taken together, these data indicate that expression of BORIS promotes a switch from a proliferative to invasive state at both the transcriptional and phenotypic level in melanoma cell lines.

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ChIP-seq analysis of subunits of meiotic cohesin complexes (mei-Cohesins) in transgenic human cancer cell lines

Project description:The study involved chromatin IP analyzed by high-throughput sequencing analysis using stable transgenic human cancer cell lines, which express Tet-inducible combinations of mei-cohesin subunits. The following individual genes and combinations of mei-cohesin subunits were expressed in human cells : STAG3, SMC1beta, STAG3+SMC1beta+REC8, and STAG3+SMC1beta+RAD21L The goal of the study was to investigate the epigenomic properties of somatic cells in response to the induction of mei-cohesin subunits using Tet-on inducible transgenes activated by an rtTA transgene and doxycicline.

2022-09-30 | GSE142746 | GEO

Small RNA (sRNA) RNA-seq analysis of BORIS/CTCFL knockdown in K562 cell line

Project description:The study involved transcriptome analysis using RNA-seq knockdown of BORIS/CTCFL gene expression in K652 cancer cell line using inducible shRNA. The K562 cell line is the only cancer cell line that is known to be dependent on BORIS for proliferation and self-renewal of stemness. The goal of the study was to investigate the early/immediate small RNA transcriptional response to BORIS downregulation (over 10-fold reduction in protein level) using an inducible shRNA.

2017-09-25 | GSE99899 | GEO

Expression data from ovarian cancer cell line OVCAR3 following Knockdown or Knockout of BORIS (CTCFL)

Project description:The identification of prognostic biomarkers is a priority for patients suffering from high-grade serous ovarian cancer (SOC), which accounts for >70% of ovarian cancer (OC) deaths. Meanwhile borderline ovarian cancer (BOC) is a low malignancy tumor and usually patients undergo surgery with low probabilities of recurrence. However, SOC remains the most lethal neoplasm due to the lack of biomarkers for early diagnosis and prognosis. In this regard BORIS (CTCFL), a CTCF paralog, is a promising cancer biomarker that is overexpressed and controls transcription in several cancer types, mainly in OC. Studies suggest that BORIS has an important function in OC by altering gene expression, but the effect and extent to which BORIS influences transcription in OC from a genome-wide perspective is unclear. Here we sought to identify BORIS target genes in an OC cell line (OVCAR3) with potential biomarker use in OC tumor samples. To achieve this, we performed in vitro knockout (KO) and knockdown (KD) experiments of BORIS in OVCAR3 cell line followed by expression microarrays and bioinformatics network enrichment analysis to identify relevant BORIS target genes.

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Project description:The aim of the experiment is to compare the transcriptional profile of MEi (mesenchymal-like mucoepidermoid tumor) cells with BM-MSCs (bone marrow mesenchymal stromal cells). The MEi cells were isolated from a mucoepidermoid tumor from the trachea. BM-MSCs were isolated from bone marrow of healthy donors. The MEi cells are a new cell line established by Dr Lim Mei Ling.

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