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CPSF1 inhibition promotes widespread use of intergenic polyadenylation sites and impairs glycolysis in prostate cancer cells [RNA-seq]

ABSTRACT: CPSF1 inhibition promotes widespread use of intergenic polyadenylation sites and impairs glycolysis in prostate cancer cells [RNA-seq]

PROVIDER: PRJNA1097251 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28579069_1.fastq.gz	Fastqsanger.gz
	SRR28579069_2.fastq.gz	Fastqsanger.gz
	SRR28579070_1.fastq.gz	Fastqsanger.gz
	SRR28579070_2.fastq.gz	Fastqsanger.gz
	SRR28579071_1.fastq.gz	Fastqsanger.gz

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CPSF1 inhibition promotes widespread use of intergenic polyadenylation sites and impairs glycolysis in prostate cancer cells [PAC-seq]

Project description:CPSF1 inhibition promotes widespread use of intergenic polyadenylation sites and impairs glycolysis in prostate cancer cells [PAC-seq]

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CPSF1 inhibition promotes widespread use of intergenic polyadenylation sites and impairs glycolysis in prostate cancer cells [RNA-seq]

Project description:The goal of this study was to compare globlal expression changes upon CPSF1 knockdown in LNCaP, LNCaP95, and 22Rv1 prostate cancer cells.

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CPSF1 inhibition promotes widespread use of intergenic polyadenylation sites and impairs glycolysis in prostate cancer cells [PAC-seq]

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Arginine methylation regulates widespread alternative polyadenylation

Project description:Alternative polyadenylation (APA) has recently been recognized as a universal mechanism for gene regulation, but it remains unclear how APA is controlled. Here we report that the Arabidopsis thaliana Protein Arginine Methyltransferase 10 (AtPRMT10) regulates global APA with its protein partner HLP1, a conserved hnRNP A/B protein. HLP1 binds preferentially to A-rich and U-rich cis-elements around polyadenylation sites, thereby linking AtPRMT10 to the control of APA through protein-protein interactions. AtPRMT10 mutations cause significant proximal-to-distal poly(A) site shifts largely overlapping with those in hlp1-1 mutants. Proximal polyadenylation is maintained by AtPRMT10-directed methylation and is mediated in part by methylation of HLP1 at specific arginine residues. Our findings demonstrate that arginine methylation of an RNA-binding protein adds a novel layer of regulation to widespread alternative polyadenylation.

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Widespread intronic polyadenylation inactivates tumor suppressor genes in leukemia

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Widespread intronic polyadenylation inactivates tumor suppressor genes in leukemia

Project description:DNA mutations are known cancer drivers. Here, we investigated if mRNA events that are upregulated in cancer can functionally mimic the outcome of genetic alterations. 3′-seq or RNA-seq were applied to normal and malignant B cells from chronic lymphocytic leukemia (CLL; N = 59). We discovered widespread upregulation of truncated mRNAs and proteins in primary CLL cells that were not generated by genetic alterations but occurred through intronic polyadenylation (IPA). IPA-generated truncated mRNAs were often recurrent (N = 330) and predominantly affected genes with tumor-suppressive functions. The IPA-generated truncated proteins often lack the tumor-suppressive functions of the corresponding full-length proteins (DICER, FOXN3), and several even acted in an oncogenic manner (CARD11, MGA, CHST11). In CLL, inactivation of tumor-suppressor genes (TSGs) through aberrant mRNA processing is substantially more prevalent than loss of TSGs through genetic events. We further identified novel TSG candidates that are inactivated by IPA in leukemia and by truncating DNA mutations in solid tumors. These genes are understudied in cancer as their overall mutation rates are lower than those of well-known TSGs. Our findings show the need to go beyond genomic analyses in cancer diagnostics, as mRNA events that are silent at the DNA level are widespread contributors to cancer pathogenesis through inactivation of TSGs.

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Project description:Alternative polyadenylation gives rise to a wide variety of mRNA isoforms with distinct 3' ends; an individual gene can yield many 3' mRNA isoforms and has a typical pattern of poly(A) site use. To identify possible determinants of polyadenylation site distribution, we have used CRISPR to create Saccharomyces cerevisiae strains harboring precise ORF deletions in candidate genes encoding various factors involved in gene expression. We have performed 3' READS to determine the genome-wide pattern of 3' mRNA isoform endpoints in these mutant strains.

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Extensive alternative polyadenylation during zebrafish development

Project description:The post-transcriptional fate of messenger RNAs (mRNAs) is largely dictated by their 3' untranslated regions (3'UTRs), which are defined by cleavage and polyadenylation (CPA) of pre-mRNAs. We used poly(A)-position profiling by sequencing (3P-Seq) to map poly(A) sites at eight developmental stages and tissues in the zebrafish. Analysis of over 60 million 3P-Seq reads substantially increased and improved existing 3'UTR annotations, resulting in confidently identified 3'UTRs for more than 78.79% of the annotated protein-coding genes in zebrafish. Most zebrafish genes undergo alternative CPA with more than a thousand genes using different dominant 3'UTRs at different stages. 3'UTRs tend to be shortest in the ovaries and longest in the brain. Isoforms with some of the shortest 3'UTRs are highly expressed in the ovary yet absent in the maternally contributed RNAs of the embryo, perhaps because their 3'UTRs are too short to accommodate a uridine-rich motif required for stability of the maternal mRNA. At two hours post-fertilization, thousands of unique poly(A) sites appear at locations lacking a typical polyadenylation signal, which suggests a wave of widespread cytoplasmic polyadenylation of mRNA degradation intermediates. Our insights into the identities, formation, and evolution of zebrafish 3'UTRs provide a resource for studying gene regulation during vertebrate development. 3P-Seq was used to map the 3' ends of protein-coding genes in the zebrafish genome

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