FUS reads histone H3K36me3 to regulate alternative polyadenylation
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ABSTRACT:
PROVIDER: PRJNA875406 | ENA |
REPOSITORIES: ENA
Similar Datasets
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 | GSE212424 | 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: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 | GSE212422 | GEO
Project description:FUS reads histone H3K36me3 to regulate alternative polyadenylation [CUT&Tag]
| PRJNA875408 | ENA
Project description:FUS reads histone H3K36me3 to regulate alternative polyadenylation [RIP-seq]
| PRJNA875417 | ENA
Project description:FUS reads histone H3K36me3 to regulate alternative polyadenylation [PolyA-seq]
| PRJNA875409 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2024-03-21 | GSE212425 | GEO
Project description:Divergence of alternative polyadenylation in mouse
| PRJEB15336 | ENA
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 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