FUS binds the CTD of RNA polymerase II and regulates its phosphorylation at Ser2

Jacob C Schwartz, Christopher C. Ebmeier, Elaine R. Podell, Joseph Heimiller, Dylan J. Taatjes, Thomas R. Cech

Research output: Contribution to journalArticle

106 Scopus citations


Mutations in the RNA-binding protein FUS (fused in sarcoma)/TLS have been shown to cause the neurodegenerative disease amyotrophic lateral sclerosis (ALS), but the normal role of FUS is incompletely understood. We found that FUS binds the C-terminal domain (CTD) of RNA polymerase II (RNAP2) and prevents inappropriate hyperphosphorylation of Ser2 in the RNAP2 CTD at thousands of human genes. The loss of FUS leads to RNAP2 accumulation at the transcription start site and a shift in mRNA isoform expression toward early polyadenylation sites. Thus, in addition to its role in alternative RNA splicing, FUS has a general function in orchestrating CTD phosphorylation during RNAP2 transcription.

Original languageEnglish (US)
Pages (from-to)2690-2695
Number of pages6
JournalGenes and Development
Issue number24
Publication statusPublished - 2012
Externally publishedYes



  • FUS
  • P-TEFb
  • RNA-binding protein
  • TLS
  • Transcription

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology

Cite this

Schwartz, J. C., Ebmeier, C. C., Podell, E. R., Heimiller, J., Taatjes, D. J., & Cech, T. R. (2012). FUS binds the CTD of RNA polymerase II and regulates its phosphorylation at Ser2. Genes and Development, 26(24), 2690-2695. https://doi.org/10.1101/gad.204602.112