de.mpg.escidoc.pubman.appbase.FacesBean
Deutsch
 
Hilfe Wegweiser Datenschutzhinweis Impressum Kontakt
  DetailsucheBrowse

Datensatz

DATENSATZ AKTIONENEXPORT

Freigegeben

Zeitschriftenartikel

CpG-depleted promoters harbor tissue-specific transcription factor binding signals—implications for motif overrepresentation analyses.

MPG-Autoren
http://pubman.mpdl.mpg.de/cone/persons/resource/persons50500

Roider,  Helge G.
Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society;

Haas,  Stefan A.
Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons50613

Vingron,  Martin
Gene regulation (Martin Vingron), Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society;

Externe Ressourcen
Es sind keine Externen Ressourcen verfügbar
Volltexte (frei zugänglich)

6305.pdf
(beliebiger Volltext), 9MB

Ergänzendes Material (frei zugänglich)
Es sind keine frei zugänglichen Ergänzenden Materialien verfügbar
Zitation

Roider, H. G., Lenhard, B., Kanhere, A., Haas, S. A., & Vingron, M. (2009). CpG-depleted promoters harbor tissue-specific transcription factor binding signals—implications for motif overrepresentation analyses. Nucleic Acids Research, 37(19), 6305-6315. doi:10.1093/nar/gkp682.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0010-7D3F-B
Zusammenfassung
Motif overrepresentation analysis of proximal promoters is a common approach to characterize the regulatory properties of co-expressed sets of genes. Here we show that these approaches perform well on mammalian CpG-depleted promoter sets that regulate expression in terminally differentiated tissues such as liver and heart. In contrast, CpG-rich promoters show very little overrepresentation signal, even when associated with genes that display highly constrained spatiotemporal expression. For instance, while ~50% of heart specific genes possess CpG-rich promoters we find that the frequently observed enrichment of MEF2-binding sites upstream of heart-specific genes is solely due to contributions from CpG-depleted promoters. Similar results are obtained for all sets of tissue-specific genes indicating that CpG-rich and CpG-depleted promoters differ fundamentally in their distribution of regulatory inputs around the transcription start site. In order not to dilute the respective transcription factor binding signals, the two promoter types should thus be treated as separate sets in any motif overrepresentation analysis.