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Modulation of m6A RNA Methylation by Death Associated Protein 3 (DAP3)

ABSTRACT: Modulation of m6A RNA Methylation by Death Associated Protein 3 (DAP3)

PROVIDER: PRJNA994439 | ENA |

REPOSITORIES: ENA

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Modulation of m6A RNA Methylation by Death Associated Protein 3 (DAP3) [eCLIP-seq]

Project description:Modulation of m6A RNA Methylation by Death Associated Protein 3 (DAP3) [eCLIP-seq]

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Modulation of m6A RNA Methylation by Death Associated Protein 3 (DAP3)

Project description:MeRIP-seq data of m6A signals in shScr control and two shDAP3 knockdown samples

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Death Associated Protein 3 (DAP3) Coordinates Splicing Regulatory Networks to Modulate Global Alternative Splicing in Cancer

Project description:The dynamic regulation of transcriptome requires coordinated participation of multiple RNA binding proteins (RBPs) in RNA processing. Dysregulated RNA processing, such as aberrant alternative splicing, is implicated in many cancers. Therefore, it is critical to explore the cancer-related RNA processing regulation and the underlying mechanisms. Many RBPs lack classical RNA-binding domains and their functions in RNA processing regulation remain unclear. Through an unbiased transcriptome-wide analysis, we report DAP3 binds ubiquitously to endogenous RNAs in vivo and its depletion reshapes the alternative splicing landscape in cancer cells. Mechanistically, we show DAP3 coordinates splicing regulatory networks, not only via mediating the formation of ribonucleoprotein (RNP) complexes, but also via modulating splicing of numerous splicing factors. Specific DAP3-regulated splicing changes such as non-productive splicing of WSB1 and RBM6, play important roles in tumorigenesis. Together, these findings provide critical mechanistic insights into the molecular functions of DAP3 in cancer development as a master regulator of RNA processing.

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Suppression of adenosine-to-inosine (A-to-I) RNA editome by death associated protein 3 (DAP3) promotes cancer progression

Project description:RNA editing introduces nucleotide changes in RNA sequences. Recent studies have reported that aberrant A-to-I RNA editing profiles are implicated in cancers. Albeit changes in expression and activity of ADAR genes are thought to have been responsible for the dysregulated RNA editome in diseases, they are not always correlated, indicating the involvement of secondary regulators. Here, we uncover DAP3 as a potent repressor of editing and a strong oncogene in cancer. DAP3 mainly interacts with the deaminase domain of ADAR2 and represses editing via disrupting association of ADAR2 with its target transcripts. PDZD7, an exemplary DAP3-repressed editing target, undergoes a protein recoding editing at stop codon [Stop →Trp (W)]. Because of editing suppression by DAP3, the unedited PDZD7WT, which is more tumorigenic than edited PDZD7Stop518W, is accumulated in tumors. In sum, cancer cells may acquire malignant properties for their survival advantage through suppressing RNA editome by DAP3.

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Modulation of m6A RNA Methylation by Death Associated Protein 3 (DAP3) [eCLIP-seq]

Project description:eCLIP-seq data of METTL3 binding in shScr control and two shDAP3 knockdown samples

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Discovery of DAP3-binding RNA sites by eCLIP

Project description:eCLIP paired-end sequencing of DAP3 in EC109 cells with two biological replicates. This analysis revealed the genome-wide RNA binding landscape of DAP3, as the supporting data of the main publication.

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Death Associated Protein 3 (DAP3) Coordinates Splicing Regulatory Networks to Modulate Global Alternative Splicing in Cancer

Project description:Death Associated Protein 3 (DAP3) Coordinates Splicing Regulatory Networks to Modulate Global Alternative Splicing in Cancer

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m6A RNA methylation promotes XIST-mediated transcriptional repression

Project description:XIST is a long non-coding RNA (lncRNA) that mediates transcriptional silencing of X chromosome genes. Here we show that XIST is highly methylated with at least 78 N6-methyladenosine (m6A) residues, a reversible base modification whose function in lncRNAs is unknown. We show that m6A formation in XIST, as well as cellular mRNAs, is mediated by RBM15 and its paralog RBM15B, which bind the m6A-methylation complex and recruit it to specific sites in RNA. This results in methylation of adenosines in adjacent m6A consensus motifs. Furthermore, knockdown of RBM15 and RBM15B, or knockdown of the m6A methyltransferase METTL3 impairs XIST-mediated gene silencing. A systematic comparison of m6A-binding proteins shows that YTHDC1 preferentially recognizes m6A in XIST and is required for XIST function. Additionally, artificial tethering of YTHDC1 to XIST rescues XIST-mediated silencing upon loss of m6A. These data reveal a pathway of m6A formation and recognition required for XIST-mediated transcriptional repression. Three to four biological HEK293T replicates were used to perform iCLIP of endogenous YTH proteins, RBM15, and RBM15B. Crosslinking induced truncations were identified using CIMS-CITS pipeline.

2016-09-07 | E-GEOD-78030 | biostudies-arrayexpress

Suppression of adenosine-to-inosine (A-to-I) RNA editome by death associated protein 3 (DAP3) promotes cancer progression

Project description:Suppression of adenosine-to-inosine (A-to-I) RNA editome by death associated protein 3 (DAP3) promotes cancer progression

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Project description:m6A is a ubiquitous RNA modification in eukaryotes. Transcriptome-wide m6A patterns in Arabidopsis have been assayed recently. However, m6A differential patterns among organs have not been well characterized. The goal of the study is to comprehensively analyze m6A patterns of numerous types of RNAs, the relationship between transcript level and m6A methylation extent, and m6A differential patterns among organs in Arabidopsis. In total, 18 libraries were sequneced. For the 3 organs: leaf, flower and root, each organ has mRNA-Seq, m6A-Seq and Input sequenced. And each sequence has 2 replicats.

2015-10-28 | E-GEOD-72706 | biostudies-arrayexpress

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