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Genome-wide DNA-binding analysis for Ttk in intestinal progenitor cells and Su(H) in wildtype, seq overexpressed and ttk-RNAi intestinal progenitor cells by DamID

ABSTRACT: Genome-wide DNA-binding analysis for Ttk in intestinal progenitor cells and Su(H) in wildtype, seq overexpressed and ttk-RNAi intestinal progenitor cells by DamID

PROVIDER: PRJNA542068 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9032290.fastq.gz	Fastqsanger.gz
	SRR9032291.fastq.gz	Fastqsanger.gz
	SRR9032282.fastq.gz	Fastqsanger.gz
	SRR9032292.fastq.gz	Fastqsanger.gz
	SRR9032283.fastq.gz	Fastqsanger.gz

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Similar Datasets

Genome-wide DNA-binding analysis for Ttk in intestinal progenitor cells and Su(H) in wildtype, seq overexpressed and ttk-RNAi intestinal progenitor cells by DamID

Project description:Purpose: Genome-wide DNA-binding analysis for Ttk in intestinal progenitor cells and comparing Su(H) binding sites between seq overexpressed and ttk-RNAi intestinal progenitor cells in Drosophila midgut by DNA adenine methyltransferase identification(DamID) Methods: Dam(Ctrl) , Ttk-Dam transgenes, Su(H)-Dam, Su(H)-Dam&seq and Su(H)-Dam&ttk-RNAi were expressed in intestinal progenitor cells by esg-Gal4.The guts within 2 days was used for DNA adenine methyltransferase identification (DamID), followed by deep sequencing analysis Results: Ttk suppresses neural specific Notch targets through suppressing Seq in intestinal progenitor cells

2021-02-23 | GSE130941 | GEO

Transcriptome profiling of Drosophila wild type and ttk-RNAi, dpn overexpressed, Nicd overexpressed and seq&Nicd overexpressed intestinal progenitor cells

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare transcriptome profiling (RNA-seq) of intestinal progenitor cells in Drosophila wild type and ttk-RNAi, dpn overexpressed, Nicd overexpressed and seq&Nicd overexpressed midguts Methods: mRNA profiles of intestinal progenitor cells isolated from 7-day-old wild-type (Ctrl) and ttk-RNAi, dpn overexpressed(dpn OE), Nicd overexpressed(Nicd OE) and seq&Nicd overexpressed(seq&Nicd OE) Drosophila midgut were generated by deep sequencing using Illumina HiSeq 2500. Results: ttk-RNAi in intestinal progenitor cells induces the expression of many neural-specific genes, including dpn and seq. Dpn ectopic expresion explains most of the ttk-RNAi expression profile change. Seq ectopic expression explains the expression of neural-specific Notch targets in the ttk-RNAi intestinal progenitor cells.

2021-02-23 | GSE130942 | GEO

Genome-wide DNA-binding analysis for Sox100B in intestinal stem cells by DamID

Project description:Purpose: Genome-wide DNA-binding analysis for Sox100B in intestinal stem cells in Drosophila midgut by DNA adenine methyltransferase identification(DamID) Methods: DNA adenine methyltransferase identification (DamID) on Sox100B driven by ESG-Gal4 Results: 5046 significant genomic binding sites, corresponding to 3182 genes were identified via iDamID following Sox100B overexpression in progenitor cells compared to WT. About a third of these genes were in the list of significantly altered genes following Sox100B overexpression and/or depletion.

2020-05-18 | GSE130304 | GEO

The insulator protein SU(HW) modulates nuclear lamina interactions of the Drosophila genome: DamID

Project description:Specific interactions of the genome with the nuclear lamina (NL) are thought to assist chromosome folding inside the nucleus and to contribute to the regulation of gene expression. High-resolution mapping has recently identified hundreds of large, sharply defined lamina-associated domains (LADs) in the human genome, and suggested that the insulator protein CTCF may help to demarcate these domains. Here, we report the detailed structure of LADs in Drosophila cells, and investigate the putative roles of five insulator proteins in LAD organization. We found that of these five proteins, only SU(HW) binds preferentially at LAD borders and at specific positions inside LADs, while GAF, CTCF, BEAF-32 and DWG are mostly absent from these regions. By knockdown and overexpression studies we demonstrate that SU(HW) weakens LAD – NL interactions by a local antagonistic effect. Our results provide insights into the evolution of LAD organization and reveal a role for SU(HW) in the regulation of genome – NL interactions. DamID experiments for Lamin, CTCF, SU(HW), GAF, DWG, and BEAF-32, and for Lamin after overexpression and after knockdown of SU(HW), were performed in Drosophila cell cultures. Samples were hybridized to 380k NimbleGen arrays with 300 bp probe spacing. Every experiment was done in duplicate in the reverse dye orientation. The supplementary file 'GSE20311_DamID_norm_mean.txt' contains the mean log2(Dam-fusion/Dam-only) values of two replicates.

2011-01-24 | E-GEOD-20311 | biostudies-arrayexpress

Control of neural daughter cell proliferation by multi-level Notch/Su(H)/E(spl)HLH signaling. (PMID: 27070787)

Project description:We expressed DamID and Flag-tagged versions of E(spl)HLH-m5, -m8 and Su(H), in Drosophila embryos and analyzed their DNA-binding by DamID-seq and ChIP-seq. The Notch pathway controls proliferation during development and in adulthood, and is frequently affected in many disorders. However, the genetic sensitivity and multi-layered transcriptional properties of the Notch pathway has made its molecular decoding challenging. Here, we address the complexity of Notch signaling with respect to proliferation, using the developing Drosophila CNS as model. We find that a Notch/Su(H)/E(spl)-HLH cascade specifically controls daughter, but not progenitor proliferation. Additionally, we find that different E(spl)-HLH genes are required in different neuroblast lineages. The Notch/Su(H)/E(spl)-HLH cascade alters daughter proliferation by regulating four key cell cycle factors: Cyclin E, String/Cdc25, E2f and Dacapo (mammalian p21CIP1/p27KIP1/p57Kip2). ChIP and DamID analysis of Su(H) and E(spl)-HLH indicates direct transcriptional regulation of the cell cycle genes, and of the Notch pathway itself. These results point to a multi-level signaling model, and may help shed light on the dichotomous proliferative role of Notch signaling in many other systems.

2019-09-11 | GSE137195 | GEO

Genome-wide DNA-binding analysis for E(spl)m8 in intestinal stem cells by DamID

Project description:Purpose: Genome-wide DNA-binding analysis for E(spl)m8 in intestinal stem cells in Drosophila midgut by DNA adenine methyltransferase identification(DamID) Methods: DNA adenine methyltransferase identification (DamID) on E(spl)m8 driven by Dl-Gal4 Results:

2018-02-02 | GSE102568 | GEO

SetDB1 and Su(var)3-9 play non-overlapping roles in somatic cell chromosomes of Drosophila melanogaster [DamID-seq]

Project description:Three distinct enzymes are known to be capable of methylating lysine 9 residue of the histone H3 in Drosophila melanogaster: Su(var)3-9, SetDB1, and G9a. Here, we explored functional specialization of the two of them: SetDB1 and Su(var)3-9. Using DamID approach, we generated the binding profile for SetDB1 in salivary gland chromosomes, and matched it to the previously published profile of Su(var)3-9. Unlike Su(var)3-9, SetDB1 is an euchromatic protein that is absent from repeated DNA compartment, and is largely restricted to TSSes and 5'UTRs of moderately active ubiquitously expressed genes. Significant SetDB1 association is also observed at or near insulator protein CP190 binding sites. Extensive, yet not exact colocalization SetDB1 with Su(var)3-9 occurs only along the chromosome 4. Importantly, SetDB1 and H3K9me2/3-enriched sites tend to display poor overlap. At the same time, SetDB1 has clear connection with the distribution of H3K27me3 mark. SetDB1 binds outside the domains possessing this modification, and about half of the borders of H3K27me3 domains are decorated by SetDB1 binding sites together with actively transcribed genes. Given that SetDB1 displays low correlation with H3K9 methylation and binds to the TSSes of active genes, that are usually nucleosome-poor, we speculate that in somatic cells, SetDB1 may contribute to the methylation of a broader set of chromosomal proteins than just H3K9. In addition, via association with insulator proteins and transcription machinery, SetDB1 can be expected to play a role in the establishment of chromatin functional domains.

2020-08-04 | GSE155579 | GEO

Targeted DamID to understand transcription factor genomic occupancy in human foetal lung progenitor cells

Project description:In order to study the genomic occupancy of transcription factors, including SOX9, ETV4 and ETV5, in human foetal lung tip progenitor cells, we have introduced Targeted DamID system via lentivirus in a human foetal lung tissue derived organoid culture (Nikolic et al., 2017). We were able to identify the corresponding TF motif enrichment and discovered a potential co-regulation function of SOX9 and ETV factors in human feotal lung progenitor cells. This study has pioneered the use of targeted DamID approach in tissue derived organoid system.

2022-04-30 | GSE189786 | GEO

Transcriptome profiling of Drosophila wild type and ttk-RNAi, dpn overexpressed, Nicd overexpressed and seq&Nicd overexpressed intestinal progenitor cells

Project description:Transcriptome profiling of Drosophila wild type and ttk-RNAi, dpn overexpressed, Nicd overexpressed and seq&Nicd overexpressed intestinal progenitor cells

| PRJNA542069 | ENA

A novel USP9X substrate TTK contributes to tumorigenesis in non-small cell lung cancer

Project description:The X-linked deubiquitinase, USP9X, is implicated in multiple cancers by targeting various substrates. Increased expression of USP9X is observed in non-small cell lung cancer (NSCLC) and is correlated with poor prognosis. However, the molecular mechanism for USP9X regulating tumor cell survival and tumorigenesis in NSCLC is less defined. In this study, chemical labeling quantitative proteomic screening was applied to analyze A549 cells with or without USP9X RNA interference, and the resulting data suggested that TTK is a potential substrate of USP9X. Further experimental evidences confirmed that USP9X stabilized TTK via direct interaction and deubiquitination of TTK. Moreover, knockdown of USP9X or TTK inhibited cell proliferation, migration and tumorigenesis, and the immunohistochemical analysis of clinical NSCLC samples showed that the protein expression levels of USP9X and TTK were significantly elevated and positively correlated in tumor tissues. In summary, our data demonstrated that the USP9X-TTK axis may play a critical role in NSCLC, and could be considered as the potential therapeutic target.

2018-05-07 | PXD007726 | Pride

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