Mouse alternative polyadenylation
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB15336 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1616690.fastq.gz | Fastqsanger.gz | |||
| ERR1616700.fastq.gz | Fastqsanger.gz | |||
| ERR1616730.fastq.gz | Fastqsanger.gz | |||
| ERR1616750.fastq.gz | Fastqsanger.gz | |||
| ERR1616691.fastq.gz | Fastqsanger.gz |
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Similar Datasets
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
Project description:Alternative polyadenylation (APA) is an important post-transcriptional modification implicated in development. Female germline stem cell (FGSC) is unipotent and capable of giving rise to oocyte. However, whether alternative polyadenylation plays a role in self-renew and cell fate determination of FGSCs remain elusive. Here, we used 3T-Seq developed in our lab to profile genome-wide 3a termini of transcripts and delineate APA sites in mouse FGSCs and explored the biological significance of APA modulation in FGSC identity.
2015-11-20 | E-MTAB-4038 | biostudies-arrayexpress
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.
2016-03-14 | GSE79157 | GEO
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
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
2014-09-05 | GSE60487 | GEO
Project description:The 3' untranslated regions (3' UTRs) of mRNAs contain cis-acting elements for posttranscriptional regulation of gene expression. Here, we report that mouse genes tend to express mRNAs with longer 3' UTRs as embryonic development progresses. This global regulation is controlled by alternative polyadenylation and coordinates with initiation of organogenesis and aspects of embryonic development, including morphogenesis, differentiation, and proliferation. Using myogenesis of C2C12 myoblast cells as a model, we recapitulated this process in vitro and found that 3' UTR lengthening is likely caused by weakening of mRNA polyadenylation activity. Because alternative 3' UTR sequences are typically longer and have higher AU content than constitutive ones, our results suggest that lengthening of 3' UTR can significantly augment posttranscriptional control of gene expression during embryonic development, such as microRNA-mediated regulation. Two biological replicates of C2C12 growth and differentiation conditions, repesctively
2010-08-31 | E-GEOD-23871 | biostudies-arrayexpress
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.
2019-01-01 | GSE69904 | GEO
Project description:Complex organisms are able to generate differential gene expression through the same set of DNA sequences in distinct cells. The communication between chromatin and RNA regulates how cells behave in tissues. However, little is known about how chromatin, especially the histone modifications, regulates RNA polyadenylation. Here, we find that FUS is recruited to chromatin by H3K36me3 at gene bodies. Once H3K36me3 is abolished, FUS is dissociated from chromatin to increase the binding with RNA, resulting in increased distal polyadenylation selections that are far from the stop codon. The H3K36me3 recognition of FUS is mediated by the proline residues in ZNF domain, mutations of which lead to reduced chromatin association of FUS, increased RNA binding of FUS, and distal polyadenylation selections. Proline mutation, which corresponds to the mutation in amyotrophic lateral sclerosis, contributes to the hyperactivation of mitochondria and hyperdifferentiation in mouse embryonic stem cells. These findings reveal FUS as an H3K36me3 reader protein that links chromatin-mediated alternative polyadenylation to human disease.
2024-03-21 | GSE212423 | GEO
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.
2024-03-12 | GSE168897 | GEO
Project description:Partial loss of CFIm25 causes aberrant alternative polyadenylation and learning deficits [mouse]
| PRJNA597918 | ENA