This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental material
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Google Scholar
Right arrow Articles by Egloff, S.
Right arrow Articles by Murphy, S.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Egloff, S.
Right arrow Articles by Murphy, S.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, July 2009, p. 4002-4013, Vol. 29, No. 14
0270-7306/09/$08.00+0     doi:10.1128/MCB.00189-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Chromatin Structure Is Implicated in "Late" Elongation Checkpoints on the U2 snRNA and β-Actin Genes{triangledown} ,§

Sylvain Egloff, Hadeel Al-Rawaf, Dawn O'Reilly, and Shona Murphy*

Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, United Kingdom

Received 10 February 2009/ Returned for modification 19 March 2009/ Accepted 7 May 2009

The negative elongation factor NELF is a key component of an early elongation checkpoint generally located within 100 bp of the transcription start site of protein-coding genes. Negotiation of this checkpoint and conversion to productive elongation require phosphorylation of the carboxy-terminal domain of RNA polymerase II (pol II), NELF, and DRB sensitivity-inducing factor (DSIF) by positive transcription elongation factor b (P-TEFb). P-TEFb is dispensable for transcription of the noncoding U2 snRNA genes, suggesting that a NELF-dependent checkpoint is absent. However, we find that NELF at the end of the 800-bp U2 gene transcription unit and RNA interference-mediated knockdown of NELF causes a termination defect. NELF is also associated 800 bp downstream of the transcription start site of the β-actin gene, where a "late" P-TEFb-dependent checkpoint occurs. Interestingly, both genes have an extended nucleosome-depleted region up to the NELF-dependent control point. In both cases, transcription through this region is P-TEFb independent, implicating chromatin in the formation of the terminator/checkpoint. Furthermore, CTCF colocalizes with NELF on the U2 and β-actin genes, raising the possibility that it helps the positioning and/or function of the NELF-dependent control point on these genes.


* Corresponding author. Mailing address: Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, United Kingdom. Phone: 44 1865 275616. Fax: 44 1865 277556. E-mail: shona.murphy{at}path.ox.ac.uk

{triangledown} Published ahead of print on 18 May 2009.

§ Supplemental material for this article may be found at http://mcb.asm.org/.


Molecular and Cellular Biology, July 2009, p. 4002-4013, Vol. 29, No. 14
0270-7306/09/$08.00+0     doi:10.1128/MCB.00189-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.