FUS reads histone H3K36me3 to regulate alternative polyadenylation [RIP-seq]
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ABSTRACT:
PROVIDER: PRJNA875417 | ENA |
REPOSITORIES: ENA
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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: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:FUS reads histone H3K36me3 to regulate alternative polyadenylation
| PRJNA875406 | ENA
Project description:FUS reads histone H3K36me3 to regulate alternative polyadenylation [CUT&Tag]
| PRJNA875408 | 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:Myogenesis is a highly orchestrated process whereby muscle precursor cells, myoblasts, develop into muscle fibers to form skeletal muscle during embryogenesis and regenerate adult muscle. Here, we studied the RNA-binding protein FUS (fused in sarcoma), which has been implicated in muscular and neuromuscular pathologies but is poorly characterized in myogenesis. Given that FUS levels declined in human and mouse models of skeletal myogenesis, and that silencing FUS enhanced myogenesis, we hypothesized that FUS might be a repressor of myogenic differentiation. Interestingly, overexpression of FUS delayed myogenesis, accompanied by slower production of muscle differentiation markers. To identify the mechanisms through which FUS inhibits myogenesis, we uncovered RNA targets of FUS by ribonucleoprotein immunoprecipitation (RIP) followed by RNA-sequencing (RNA-seq) analysis. Stringent selection of the bound transcripts uncovered Tnnt1 mRNA, encoding troponin T (TNNT1), as a major effector of FUS influence on myogenesis. We found that in myoblasts, FUS sequestered Tnnt1 mRNA in the nucleus, preventing TNNT1 expression; however, reduction of FUS during myogenesis or by silencing FUS released Tnnt1 mRNA for export to the cytoplasm, where it accumulated and was translated into TNNT1, promoting myogenesis. We propose that FUS inhibits myogenesis by suppressing TNNT1 expression through a mechanism of nuclear mRNA retention.
2024-09-13 | GSE267277 | GEO
Project description:The aim of our study is to identify the role of FUS in shaping the transcriptome. RNA-seq of two FUS KO clones was performed and compared to wt; for each, four replicates were sequenced. RNA molecules associated with the FUS protein were determined by means of a RNA immuno-precipitation, followed by high-throughput sequencing. Total RNA was used as a control. SH-SY5Y cells were used for both experiments. RNA-seq: 4 wt samples, 4 A4 KO samples, 4 A5 KO samples. RIP-seq: 1 input control sample, 3 anti-FUS IP replicates.
2016-06-13 | E-GEOD-71812 | biostudies-arrayexpress
Project description:Divergence of alternative polyadenylation in mouse
| PRJEB15336 | ENA