Genome Res. 2009 Aug 3. [Epub ahead of print]
Access the most recent version at doi:10.1101/gr.094144.109
This manuscript is Open Access.
http://genome.cshlp.org/content/early/2009/07/31/gr.094144.109.long

"Distinguishing direct versus indirect transcription factor-DNA interactions".

Raluca Gordân 1, Alexander J. Hartemink 1, and Martha L. Bulyk 2, 3, 4, @

1 Duke University, Dept. of Computer Science, Box 90129, Durham, NC 27708, USA.
2 Division of Genetics, Department of Medicine, and 3 Department of Pathology, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115, USA.
4 Harvard-MIT Division of Health Sciences and Technology (HST), Harvard Medical School,
Boston, MA 02115, USA.

@To whom correspondence should be addressed. Email: mlbulyk@receptor.med.harvard.edu



Abstract:

Transcriptional regulation is largely enacted by transcription factors (TFs) binding DNA.
Large numbers of TF binding motifs have been revealed by ChIP-chip experiments
followed by computational DNA motif discovery. However, the success of motif discovery
algorithms has been limited when applied to sequences bound in vivo (such as those
identified by ChIP-chip) because the observed TF-DNA interactions are not necessarily
direct: some TFs predominantly associate with DNA indirectly through protein partners,
while others exhibit both direct and indirect binding. Here, we present the first method for
distinguishing between direct and indirect TF-DNA interactions, integrating in vivo TF
binding data, in vivo nucleosome occupancy data, and motifs from in vitro protein binding
microarray experiments. When applied to yeast ChIP-chip data, our method reveals that
only 48% of the data sets can be readily explained by direct binding of the profiled TF,
while 16% can be explained by indirect DNA binding. In the remaining 36%, none of the
motifs used in our analysis was able to explain the ChIP-chip data, either because the data
were too noisy or because the set of motifs was incomplete. As more in vitro TF DNA
binding motifs become available, our method could be used to build a complete catalog of
direct and indirect TF-DNA interactions. Our method is not restricted to yeast or to ChIPchip
data, but can be applied in any system for which both in vivo binding data and in vitro
DNA binding motifs are available.



Additional References:

1. Todd Wasson, and Alexander J. Hartemink, (August, 2009),
"An ensemble model of competitive multi-factor binding of the genome."

2. Frenster JH, and Hovsepian JA,  (December, 2008),
"Models of successive levels of resolution during individual gene transcription".



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Further Topics in:  Euchromatin,  active DNA, and  RNA  ribo-regulators:

Links to Current Research in Euchromatin:
Links to Euchromatin Activator RNA Reviews:
Links to Euchromatin Activator RNA Research:
Links to Ultrastructural Probes of DNase I-Sensitive Sites:
Links to RNA as a Therapeutic Agent:
Links to Hodgkin Lymphoma Immuno-Pathology:
Links to Activated T-Lymphocyte Immunotherapy:
Links to Medical Systems Biology:
Links to Selective Gene Transcription:
Links to RNA-Induced Epigenetics:
Links to RNA-Induced Embryogenesis:
Links to RNA and Biological Causality:
Links to Reprogramming and Neoplasia:

A Brief History of Activator RNA:

"Ultrastructural Probes of Active DNA Sites, and the RNA Activators of DNA".
(PowerPoint Presentation).


Top of Page - Euchromatin NetworkEuchromatin ResearchResearch in Quantitative Radiology


For Further Information and Feedback:

Jeannette A. Hovsepian, M.D.
E-mail: frensasc@ix.netcom.com
Phone:  +1 650 367 6483



euchromatin: "the most active portion of the genome within the cell nucleus".
embryoma:  "adult neoplasm expressing one or more embryo-exclusive genes".