| First Author | Lin S | Year | 2008 |
| Journal | Nat Struct Mol Biol | Volume | 15 |
| Issue | 8 | Pages | 819-26 |
| PubMed ID | 18641664 | Mgi Jnum | J:245360 |
| Mgi Id | MGI:5918739 | Doi | 10.1038/nsmb.1461 |
| Citation | Lin S, et al. (2008) The splicing factor SC35 has an active role in transcriptional elongation. Nat Struct Mol Biol 15(8):819-26 |
| abstractText | Mounting evidence suggests that transcription and RNA processing are intimately coupled in vivo, although each process can occur independently in vitro. It is generally thought that polymerase II (Pol II) C-terminal domain (CTD) kinases are recruited near the transcription start site to overcome initial Pol II pausing events, and that stably bound kinases facilitate productive elongation and co-transcriptional RNA processing. Whereas most studies have focused on how RNA processing machineries take advantage of the transcriptional apparatus to efficiently modify nascent RNA, here we report that a well-studied splicing factor, SC35, affects transcriptional elongation in a gene-specific manner. SC35 depletion induces Pol II accumulation within the gene body and attenuated elongation, which are correlated with defective P-TEFb (a complex composed of CycT1-CDK9) recruitment and dramatically reduced CTD Ser2 phosphorylation. Recombinant SC35 is sufficient to rescue this defect in nuclear run-on experiments. These findings suggest a reciprocal functional relationship between the transcription and splicing machineries during gene expression. |
