FUS binds the CTD of RNA polymerase II and regulates its phosphorylation at Ser2
作者： J. C. Schwartz , C. C. Ebmeier , E. R. Podell , J. Heimiller , D. J. Taatjes
关键词: Transcription (biology) 、 RNA-binding protein 、 Biology 、 P-TEFb 、 Alternative splicing 、 Gene isoform 、 RNA polymerase II 、 Molecular biology 、 Messenger RNA 、 Polyadenylation
摘要: Mutations in the RNA-binding protein FUS (fused sarcoma)/TLS have been shown to cause neurodegenerative disease amyotrophic lateral sclerosis (ALS), but normal role of is incompletely understood. We found that binds C-terminal domain (CTD) RNA polymerase II (RNAP2) and prevents inappropriate hyperphosphorylation Ser2 RNAP2 CTD at thousands human genes. The loss leads accumulation transcription start site a shift mRNA isoform expression toward early polyadenylation sites. Thus, addition its alternative splicing, has general function orchestrating phosphorylation during transcription.
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