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U6 snRNP inhibits the premature cleavage and polyadenylation of pre-mRNAs

ABSTRACT: U6 snRNP inhibits the premature cleavage and polyadenylation of pre-mRNAs

PROVIDER: PRJNA1053386 | ENA |

REPOSITORIES: ENA

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U6 snRNP inhibits the premature cleavage and polyadenylation of pre-mRNAs (3'-Seq)

Project description:To investigate the extent to which U6 inhibits premature cleavage and polyadenylation at the transcriptome level. we performed 3’-seq in control, U1 and U6-AMO treated sample using lexogen 3’-seq kit (Cat. 016.24) that could accurately quantify the global PAS usage. Indeed, we found both U1 and U6 could globally suppress intronic PCPA.

2025-01-29 | GSE250342 | GEO

U6 snRNP inhibits the premature cleavage and polyadenylation of pre-mRNAs (ChIP-Seq)

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U4 inhibits premature cleavage and polyadenylation of pre-mRNAs [ChIP-seq]

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U4 inhibits premature cleavage and polyadenylation of pre-mRNAs [mRNA-seq]

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U6 snRNP inhibits the premature cleavage and polyadenylation of pre-mRNAs (ChIP-Seq)

Project description:RNAPII ChIP-seq analysis in U2 and U6 antisense morpholino oligonucleotide (AMO)-treated HeLa cells in comparison to negative control (NC) AMO To investigate if U2 or U6 AMO treatment caused transcription defect, we carried out RNAPII ChIP-seq analysis in control, U2 and U6 AMO treated HeLa cells

2025-01-29 | GSE250343 | GEO

U6 snRNP inhibits the premature cleavage and polyadenylation of pre-mRNAs (RNA-Seq)

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U4 inhibits premature cleavage and polyadenylation of pre-mRNAs [mRNA 3'-seq]

Project description:To understand how U4 snRNP regulates premature cleavage and polyadenylation of pre-mRNAs at the transcriptome wide, we conducted 3'-seq analysis on control, U1 and U4-AMO treated samples using the Lexogen mRNA 3'-seq kit (Cat. 016.24), which enables accurate quantification of global PAS usage.

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U1 snRNP complex with cleavage and polyadenylation factors controls mRNA transcription termination

Project description:Full-length transcription in the majority of human genes depends on U1 snRNP (U1) to co-transcriptionally suppress transcription-terminating premature 3’-end cleavage and polyadenylation (PCPA) from cryptic polyadenylation signals (PASs) in introns. However, the mechanism of this U1 activity, termed telescripting, is unknown. Here, we captured a complex, comprising U1 and CPA factors (U1–CPAFs), that binds intronic PASs and suppresses PCPA. U1–CPAFs are distinct from U1-spliceosomal complexes; they include CPA’s three main subunits, CFIm, CPSF, and CstF, lack essential splicing factors, and associate with transcription elongation and mRNA export complexes. Telescripting requires U1:pre-mRNA base-pairing, which can be disrupted by U1 antisense oligonucleotide (U1 AMO), triggering PCPA. U1 AMO remodels U1–CPAFs, revealing changes, including recruitment of CPA-stimulating factors, that explain U1–CPAFs’ switch from repressive to activated states. Our findings outline U1 telescripting mechanism and demonstrate U1’s unique role as central-regulator of pre-mRNA processing and transcription.

2019-07-31 | GSE135140 | GEO

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