Brief Communication abstract
Nature Genetics 39, 730 - 732 (2007)
Published online: 21 May 2007 | doi:10.1038/ng2047
Tissue-specific transcriptional regulation has diverged significantly between human and mouse
Duncan T Odom1,5,6, Robin D Dowell2,6, Elizabeth S Jacobsen1, William Gordon3, Timothy W Danford2, Kenzie D MacIsaac4, P Alexander Rolfe2, Caitlin M Conboy1,5, David K Gifford1,2 & Ernest Fraenkel2,3
We demonstrate that the binding sites for highly conserved transcription factors vary extensively between human and mouse. We mapped the binding of four tissue-specific transcription factors (FOXA2, HNF1A, HNF4A and HNF6) to 4,000 orthologous gene pairs in hepatocytes purified from human and mouse livers. Despite the conserved function of these factors, from 41% to 89% of their binding events seem to be species specific. When the same protein binds the promoters of orthologous genes, approximately two-thirds of the binding sites do not align.
- Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA.
- Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
- Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
- Department of Electrical Engineering and Computer Science, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
- Present address: Cancer Research UK–Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK.
- These authors contributed equally to this work.
Correspondence to: Ernest Fraenkel2,3 e-mail: fraenkel-admin@mit.edu
MORE ARTICLES LIKE THIS
These links to content published by NPG are automatically generated.
RESEARCH
Treatment of opioid-induced constipation with oral naloxone: A pilot studyClinical Pharmacology and Therapeutics Original Article
A burst of segmental duplications in the genome of the African great ape ancestorNature Letters to Editor (12 Feb 2009)
The gene mutated in autosomal recessive polycystic kidney disease encodes a large, receptor-like proteinNature Genetics Article (01 Mar 2002)

