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Alternative intronic polyadenylation influences cancer metastasis and response to therapy [3'-seq]

ABSTRACT: We explored the impact of alternative polyadenylation regulation during tumor cell spreading.

ORGANISM(S): Mus musculus

PROVIDER: GSE94373 | GEO | 2018/01/01

SECONDARY ACCESSION(S): PRJNA369527

REPOSITORIES: GEO

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Alternative intronic polyadenylation influences cancer metastasis and response to therapy

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Alternative intronic polyadenylation influences cancer metastasis and response to therapy

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Genome-wide profiling of Alternative polyadenylation sites in mouse female germline stem cells

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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

RSC and Bud27 influences chromatin organization and alternative polyadenylation

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

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Alternative polyadenylation is a minor feature of primary human muscle differentiation

Project description:Alternative polyadenylation has been explored in multiple native and disease transitions. The prevailing hypothesis being that differentiated cells use longer 3’UTRs with more scope for regulation, whereas undifferentiated cells use shorter, less regulated 3’UTRs. Here we describe gene-expression and alternative polyadenylation of human primary myocytes over a time course differentiation. Contrary to expectation, only minor changes to 3’-end choice were detected. To reconcile this finding with published differentiation data in the immortalized C2C12 myocyte cell line, a systematic comparison was undertaken. Less than half the genes differentially expressed in the immortalized model were recapitulated in primary cells, and of these, important metabolic states were either absent, underrepresented or regulated in the opposite direction. A new bioinformatic approach, developed to quantitate the degree of alternative polyadenylation between unrelated experiments demonstrated that alternative polyadenylation was reduced by ~50% with less than 1/10 of the genes that underwent alternative polyadenylation in C2C12 differentiation showing alternative processing in primary muscle differentiation. A possible explanation for this difference was a less pronounced down regulation of the cleavage and polyadenylation factors in the differentiation primary cell. In sum, the data promote the use of primary human myocytes to model muscle biogenesis over immortalized models that may not fully recapitulate human muscle development.

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