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CPSF6 regulates alternative polyadenylation and proliferation of cancer cell through phase separation

ABSTRACT: CPSF6 regulates alternative polyadenylation and proliferation of cancer cell through phase separation

PROVIDER: PRJNA967743 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24455600.fastq.gz	Fastqsanger.gz
	SRR24455601.fastq.gz	Fastqsanger.gz
	SRR24455602.fastq.gz	Fastqsanger.gz
	SRR24455603.fastq.gz	Fastqsanger.gz
	SRR24455604.fastq.gz	Fastqsanger.gz

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CPSF6 regulates alternative polyadenylation and proliferation of cancer cell through phase separation

Project description:In order to explore the impact of phase separation of CPSF6 on APA, we identified the structural domains that affect its phase separation formation and performed mutations. In addition, we also found that the phosphorylation of CPSF6 can also affect its phase separation effect, and identified key kinases. We performed IVT-SAPAS sequencing on both cases mentioned above.

2023-09-03 | GSE231823 | GEO

CPSF6 regulates alternative polydenylation and proliferation of cancer cell through phase separation Ⅱ

Project description:To verify the effect of phosphorylation of CPSF6 by CLK2 on APA, we co overexpressed CLK2 and wild-type CPSF6 or phosphorylated mutant CPSF6 in HEK293T cells

2024-08-15 | GSE230813 | GEO

CPSF6 regulates alternative polydenylation and proliferation of cancer cell through phase separation Ⅱ

Project description:CPSF6 regulates alternative polydenylation and proliferation of cancer cell through phase separation Ⅱ

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Phosphorylation of CPSF6 RS-like domain

Project description:Cleavage factor I mammalian (CFIm) complex, composed of cleavage and polyadenylation specificity factor CPSF6, regulates alternative polyadenylation (APA). CPSF6 has a RS-like domain which plays role in protein -protein interactions. This interaction might have role in alternative polyadenylation site selection. The phosphorylation of RS- like domain might play role in protein -protein interaction and thus might have a role in alternative polyadenylation site selection. So we did mass specteroanalysis to analyse phosphorylation sites of RS-like domain of CPSF6.

2019-04-01 | PXD012713 | Pride

Loss of MBNL Leads to Disruption of Developmentally Regulated Alternative Polyadenylation in RNA-Mediated Disease

Project description:Mapping MBNL-regulated genome-wide alternative polyadenylation: We report that depletion of Mbnl proteins in mouse embryo fibroblasts (MEFs), DM mouse model quadriceps muscle, and DM-autopsy muscle tissue leads to mis-regulation of alternative polyadenylation We compared WT, Mbnl1/2KO, Mbnl1/2KO/3siRNA, and Mbnl1/2KO/scrambled siRNA MEFs (n=2 for each group) to evaluate alternative polyadenylation shifts that occur due to progressive loss of Mbnl proteins. We also compared WT (1 day old, and 4 months old, n=2 each) and HSALR mouse model (4 months old, n=2) of myotonic dystrophy for developmental alternative polyadenylation defects in myotonic dystrophy. Finally, we compared control and DM1 autopsy muscle tissues (n=3) for changes in alternative polyadenylation. We performed HITS-CLIP analysis of binding sites of Mbnl1, Mbnl2 and Mbnl3 in MEFs (n=3 each). We also performed HITS-CLIP analysis for major skeletal muscle Mbnl protein, Mbnl1 in FVB WT adult muscle (4 months, n=3). Finally we performed HITS-CLIP analysis for CPSF6 in WT and Mbnl1/2 KO MEFs (n=3 each) Please note that the 'readme_Table.txt' describes the contents of 'Table S*.xlsx' files, and the readme_method.txt include additional details about experiemenal procedures.

2014-09-05 | E-GEOD-60487 | biostudies-arrayexpress

Mouse alternative polyadenylation

Project description:Divergence of alternative polyadenylation in mouse

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Alternative polyadenylation factor CPSF6 regulates temperature compensation of the mammalian circadian clock

Project description:A defining property of circadian clocks is temperature compensation, characterized by the resilience of circadian free-running periods against changes in environmental temperature.We quantify global changes in 3´UTR length as well as gene and protein expression between wild type and CPSF6 knock-down cells and their dependency on temperature.

2023-05-23 | PXD029343 | Pride

Coupling between alternative polyadenylation and alternative splicing is limited to terminal introns

Project description:Alternative polyadenylation has been implicated as an important regulator of gene expression. In some cases, alternative polyadenylation is known to couple with alternative splicing to influence last intron removal. However, it is unknown whether alternative polyadenylation events influence alternative splicing decisions at upstream exons. Knockdown of the polyadenylation factors CFIm25 or CstF64 was used as an approach in identifying alternative polyadenylation and alternative splicing events on a genome-wide scale. Although hundreds of alternative splicing events were found to be differentially spliced in the knockdown of CstF64, genes associated with alternative polyadenylation did not exhibit an increased incidence of alternative splicing. These results demonstrate that the coupling between alternative polyadenylation and alternative splicing is usually limited to defining the last exon. The striking influence of CstF64 knockdown on alternative splicing can be explained through its effects on UTR selection of known splicing regulators such as hnRNP A2/B1, thereby indirectly influencing splice site selection. We conclude that changes in the expression of the polyadenylation factor CstF64 influences alternative splicing through indirect effects. HeLa cell line was stably transfected with shRNA plasmids targeting CstF64. Total RNA was isolated from CstF64 KD cells and wild-type control cells using Trizol according to manufacturerâs protocols. Samples were deep sequenced in duplicate using the Illumina GAIIx system.

2016-03-14 | E-GEOD-79157 | biostudies-arrayexpress

Loss of CPSF6 causes developmental disease via bimodal changes in polyadenylation site usage and protein expression [Zebrafish]

Project description:Most pre-messenger RNA (pre-mRNA) undergo extensive processing to create distinct transcripts from the same gene. One of these processes, alternative polyadenylation, involves over twenty proteins to bind and cleave the pre-mRNA at poly(A) sites that can lie within the 3' UTR, introns, or exons; this can modulate protein function, but the effect of choosing a site internal to the gene vs. within the 3' UTR remains unclear. Here we show that reduced expression of CPSF6, one of the proteins involved in site selection, derails development in both humans and zebrafish by causing a bidirectional shift in poly(A) site usage. CPSF6 insufficiency favors the use of intronic poly(A) sites in neuronal genes, reducing mRNA and protein abundance, but promotes 3' UTR site usage in cardiovascular and skeletal genes, upregulating mRNA and protein.These data thus provides a long-sought link between APA and gene expression and shows that poly(A) site selection influences development.

2023-01-15 | GSE206558 | GEO

Loss of CPSF6 causes developmental disease via bimodal changes in polyadenylation site usage and protein expression [Human]

Project description:Most pre-messenger RNA (pre-mRNA) undergo extensive processing to create distinct transcripts from the same gene. One of these processes, alternative polyadenylation, involves over twenty proteins to bind and cleave the pre-mRNA at poly(A) sites that can lie within the 3' UTR, introns, or exons; this can modulate protein function, but the effect of choosing a site internal to the gene vs. within the 3' UTR remains unclear. Here we show that reduced expression of CPSF6, one of the proteins involved in site selection, derails development in both humans and zebrafish by causing a bidirectional shift in poly(A) site usage. CPSF6 insufficiency favors the use of intronic poly(A) sites in neuronal genes, reducing mRNA and protein abundance, but promotes 3' UTR site usage in cardiovascular and skeletal genes, upregulating mRNA and protein.These data thus provide a long-sought link between APA and gene expression and shows that poly(A) site selection influences development.

2023-01-15 | GSE206557 | GEO

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