1
ORAL PRESENTATION Open Access Control of LTR transcription by SWI/SNF BAF and PBAF complexes Irene Guendel 1 , Rachel Van Duyne 1,2 , Fatah Kashanchi 1,2* From 16th International Conference on Human Retroviruses: HTLV and Related Viruses Montreal, Canada. 26-30 June 2013 The transcription of HTLV-1 LTR is a highly regulated process by the organized chromatin structure within a cells nucleus; chromatin is folded into compact fibers (30-400 nm thick), which physically prevents the acces- sibility of cellular promoters by transcriptional machin- ery. A variety of enzymes and protein complexes are present in the cell to mediate the openingand closingof chromatin structure to allow for viral and cellular processes to occur. This chromatin remodeling occurs through two major mechanisms: covalent epigenetic modifications of N-terminal histone tails and ATP- dependent chromatin remodeling complexes (CRCs). HTLV-1 Tax has been shown by us and others to effec- tively regulate both steps. Here, we will discuss the effect of BAF and PBAF using a series of siRNA experi- ments for both basal and activated transcription. We observed that BAF complexes are regulated by phos- phorylation of Baf 53 subunit (possibly by pTEF-b) and PBAF complexes substitute the negative inhibitory BAF complexes needed for activated transcription. We believe that Baf 53 activity is through closing of the chromatin structure at the transcription start site and that PBAF is able to aid in elongation by communicat- ing with p300/PCAF and histone acetylated tails. Impli- cations of these complexes in transcription for both viral and cellular genes will be discussed. Authorsdetails 1 School of Systems Biology, National Center for Biodefense & Infectious Diseases, George Mason University, Manassas, Virginia, USA. 2 Department of Microbiology, Immunology, & Tropical Medicine, The George Washington University Medical Center, Washington, D.C., USA. Published: 7 January 2014 doi:10.1186/1742-4690-11-S1-O47 Cite this article as: Guendel et al.: Control of LTR transcription by SWI/ SNF BAF and PBAF complexes. Retrovirology 2014 11(Suppl 1):O47. Submit your next manuscript to BioMed Central and take full advantage of: Convenient online submission Thorough peer review No space constraints or color figure charges Immediate publication on acceptance Inclusion in PubMed, CAS, Scopus and Google Scholar Research which is freely available for redistribution Submit your manuscript at www.biomedcentral.com/submit * Correspondence: [email protected] 1 School of Systems Biology, National Center for Biodefense & Infectious Diseases, George Mason University, Manassas, Virginia, USA Full list of author information is available at the end of the article Guendel et al. Retrovirology 2014, 11(Suppl 1):O47 http://www.retrovirology.com/content/11/S1/O47 © 2014 Guendel et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Page 1: Control of LTR transcription by SWI/SNF BAF and PBAF complexes

ORAL PRESENTATION Open Access

Control of LTR transcription by SWI/SNF BAF andPBAF complexesIrene Guendel1, Rachel Van Duyne1,2, Fatah Kashanchi1,2*

From 16th International Conference on Human Retroviruses: HTLV and Related VirusesMontreal, Canada. 26-30 June 2013

The transcription of HTLV-1 LTR is a highly regulatedprocess by the organized chromatin structure within acell’s nucleus; chromatin is folded into compact fibers(30-400 nm thick), which physically prevents the acces-sibility of cellular promoters by transcriptional machin-ery. A variety of enzymes and protein complexes arepresent in the cell to mediate the opening” and “closing”of chromatin structure to allow for viral and cellularprocesses to occur. This chromatin remodeling occursthrough two major mechanisms: covalent epigeneticmodifications of N-terminal histone tails and ATP-dependent chromatin remodeling complexes (CRCs).HTLV-1 Tax has been shown by us and others to effec-tively regulate both steps. Here, we will discuss theeffect of BAF and PBAF using a series of siRNA experi-ments for both basal and activated transcription. Weobserved that BAF complexes are regulated by phos-phorylation of Baf 53 subunit (possibly by pTEF-b) andPBAF complexes substitute the negative inhibitory BAFcomplexes needed for activated transcription. Webelieve that Baf 53 activity is through closing of thechromatin structure at the transcription start site andthat PBAF is able to aid in elongation by communicat-ing with p300/PCAF and histone acetylated tails. Impli-cations of these complexes in transcription for bothviral and cellular genes will be discussed.

Authors’ details1School of Systems Biology, National Center for Biodefense & InfectiousDiseases, George Mason University, Manassas, Virginia, USA. 2Department ofMicrobiology, Immunology, & Tropical Medicine, The George WashingtonUniversity Medical Center, Washington, D.C., USA.

Published: 7 January 2014

doi:10.1186/1742-4690-11-S1-O47Cite this article as: Guendel et al.: Control of LTR transcription by SWI/SNF BAF and PBAF complexes. Retrovirology 2014 11(Suppl 1):O47.

Submit your next manuscript to BioMed Centraland take full advantage of:

• Convenient online submission

• Thorough peer review

• No space constraints or color figure charges

• Immediate publication on acceptance

• Inclusion in PubMed, CAS, Scopus and Google Scholar

• Research which is freely available for redistribution

Submit your manuscript at www.biomedcentral.com/submit

* Correspondence: [email protected] of Systems Biology, National Center for Biodefense & InfectiousDiseases, George Mason University, Manassas, Virginia, USAFull list of author information is available at the end of the article

Guendel et al. Retrovirology 2014, 11(Suppl 1):O47http://www.retrovirology.com/content/11/S1/O47

© 2014 Guendel et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the CreativeCommons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, andreproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.