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Genome-wide identification of long noncoding RNA and their potential interactors in ISWI mutants

ABSTRACT: Genome-wide identification of long noncoding RNA and their potential interactors in ISWI mutants

PROVIDER: PRJNA830770 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18888469_1.fastq.gz	Fastqsanger.gz
	SRR18888469_2.fastq.gz	Fastqsanger.gz
	SRR18888470_1.fastq.gz	Fastqsanger.gz
	SRR18888470_2.fastq.gz	Fastqsanger.gz
	SRR18888471_1.fastq.gz	Fastqsanger.gz

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Genome-wide identification of long noncoding RNA and their potential interactors in ISWI mutants

Project description:Long non-coding RNA (lncRNA) refers to non-coding RNA transcripts with a length of more than 200 nt. They regulate the expression level of target genes. However, the role of lncRNA in chromatin remodeling needs to be further explored. In this study, we used ISWI mutants (ISWI is a chromatin remodeling factor in Drosophila) to explore the function of lncRNA. Based on the transcriptome of ISWI mutant Drosophila, we analyzed the transcripts and conducted differential expression analysis. In ISWI mutants, the expression changes of lncRNAs were more significant. Our results provide a new perspective for understand the possible regulatory role of lncRNA in chromatin remodeling and identify possible lncRNA target genes in ISWI mutants.

2022-06-24 | GSE201291 | GEO

Genome-Wide Identification of Long Noncoding RNA and Their Potential Interactors in <i>ISWI</i> Mutants.

Project description:Long non-coding RNAs (lncRNAs) have been identified as key regulators of gene expression and participate in many vital physiological processes. Chromatin remodeling, being an important epigenetic modification, has been identified in many biological activities as well. However, the regulatory mechanism of lncRNA in chromatin remodeling remains unclear. In order to characterize the genome-wide lncRNA expression and their potential interacting factors during this process in Drosophila, we investigated the expression pattern of lncRNAs and mRNAs based on the transcriptome analyses and found significant differences between lncRNAs and mRNAs. Then, we performed TSA-FISH experiments of candidate lncRNAs and their potential interactors that have different functions in Drosophila embryos to determine their expression pattern. In addition, we also analyzed the expression of transposable elements (TEs) and their interactors to explore their expression in ISWI mutants. Our results provide a new perspective for understanding the possible regulatory mechanism of lncRNAs and TEs as well as their targets in chromatin remodeling.

| S-EPMC9181106 | biostudies-literature

Assessment Of Long Noncoding RNA CCAT1 In Colorectal Cancer Patients

Project description:1. Evaluate the diagnostic value of long noncoding RNA (CCAT1) expression by RT-PCR in peripheral blood in colorectal cancer patients versus normal healthy control personal. 2. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in diagnosis of colorectal cancer patients & its relation to tumor staging. 3. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in precancerous colorectal diseases. 4. Compare long noncoding RNA (CCAT1) expression with traditional marker; carcinoembryonic antigen (CEA) and Carbohydrate antigen 19-9 (CA19-9) in diagnosis of colorectal cancer.

| 2330122 | ecrin-mdr-crc

Gene expression profiling of ISWI chromatin remodeler mutants before and after DNA damage

Project description:Gene expression profiling of ISWI chromatin remodeler mutants before and after DNA damage BAZ1A is a regulatory subunit within the ISWI family of chromatin remodelers in humans. We and others have shown that BAZ1A is required for efficient recovery from DNA damage. The DNA damage hypersensitivity caused by BAZ1A* is as severe as the deletion of the entire gene. This is striking given that BAZ1A* contains only two substitutions (K1181A and K1183Y) within a poorly characterized domain of BAZ1A. We find that this domain can interact with DNA, and that the mutations present in BAZ1A* hinder DNA binding. We used transcriptional profiling to identify molecular events leading to the DNA damage hypersensitivity of BAZ1A* cells.

2017-07-06 | GSE95227 | GEO

ChIP-Seq sequencing of novel interactors of H3K4me3, H3K36me3 and H3K9me3

Project description:This study describes the epigenetic profiling of the novel interactors of H3K4me3, H3K36me3 or H3K9me3. The interactors were ChIP-Seq profiled by their GFP tag in stably transfected HeLa (Kyoto) cells. The interactors include GATAD1, Sgf29, BAP18, TRRAP, PHF8, N-PAC and LRWD1 (including replicates), as well as an GFP ChIP-Seq profile on non-transfected HeLa cells (negative control). Also included are the profiles of the histone modifications themselves (H3K4me3, H3K27me3, H3K9me3, H3K36me3, H3K9/14Ac and H3K79me3) ChIP-Seq profiling of 8 proteins by their GFP tag in stably transfected cells HeLa (Kyoto) cells, 6 replicas, as well as ChIP-Seq profiling of 6 histone modifications in wt HeLa (Kyoto) cells

2010-09-17 | E-GEOD-20303 | biostudies-arrayexpress

Affinity Purification of ISWI chromatin remodeler in Trypanosoma cruzi

Project description:Chromatin remodeling is a general mechanism involved in DNA-dependent processes, including gene expression regulation. ISWI ATPase is the catalytic subunit in diverse chromatin remodeling complexes that changing histone–DNA interactions and therefore play a pivotal role in different nuclear processes. Here, the ISWI remodeler was fused to GFP (NH and CO fusions) and its partners were determined by affinity purification-mass spectrometry (MS) assay. This approach identified known ISWI partners (NLP, RCCP and FYRP), previously characterized in T. brucei, and new components of TcISWI complex (DRBD2, DHH1 and proteins containing SMC domains).

2020-05-22 | PXD017869 | Pride

CTCF/CP190 and ISWI dependent regulation of nucleosome occupancy [MNase-seq]

Project description:MNase-seq was performed in order to analyze changes in nucleosomal occupancy after depletion of CTCF/P190 and ISWI from Drosophila S2 cells MNase-seq from Drosophila S2 nuclei after CTCF/CP190 or ISWI-specific RNAi treatment

2014-08-11 | E-GEOD-51599 | biostudies-arrayexpress

CTCF/CP190 and ISWI dependent regulation of nucleosome occupancy [ChIP-seq]

Project description:H3-ChIP-seq was performed in order to analyze changes in nucleosomal occupancy after depletion of CTCF/P190 and ISWI from Drosophila S2 cells Histone H3 ChIP-seq from Drosophila S2 cells after CTCF/CP190 or ISWI-specific RNAi treatment

2014-08-11 | E-GEOD-51598 | biostudies-arrayexpress

RNAi profiling of Drosophila SL2 cells knocked down for ISWI

Project description:Profiling of changes in steady state RNA levels upon RNAi-mediated knockdown of the nucleosome remodeling ATPase ISWI in Drosophila SL2 cells. Quantitation of the corresponding proteomes has been performed to describe transcriptome-proteome relations. The analysis indicates a limited correlation of the two expression steps. Experiment Overall Design: Drosophila SL2 cells were incubated 7 days after treatment with 10 ug of dsRNA directed against GST or ISWI, respectively. 3 biological replicates per experimental conditions have been collected.

2008-10-25 | E-GEOD-11164 | biostudies-arrayexpress

Expansion of the ISWI chromatin remodeler family with new active complexes

Project description:ISWI chromatin remodelers mobilize nucleosomes to control DNA accessibility. Complexes isolated to date pair one of six regulatory subunits with one of two highly similar ATPases. However, we find that each endogenously expressed ATPase copurifies with every regulatory subunit, substantially increasing the diversity of ISWI complexes, and we additionally identify BAZ2B as a novel, seventh regulatory subunit. Through reconstitution of catalytically active human ISWI complexes, we demonstrate that the new interactions described here are stable and direct. Finally, we profile the nucleosome remodeling functions of the now expanded family of ISWI chromatin remodelers. By revealing the combinatorial nature of ISWI complexes, we provide a basis for better understanding ISWI function in normal settings and disease.

2017-06-03 | MSV000081134 | MassIVE

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