English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Translational regulation shapes the molecular landscape of complex disease phenotypes

MPS-Authors
/persons/resource/persons50198

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

/persons/resource/persons50613

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

External Resource
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)

Schafer.pdf
(Publisher version), 858KB

Supplementary Material (public)
There is no public supplementary material available
Citation

Schafer, S., Adami, E., Heinig, M., Rodrigues, K. E., Kreuchwig, F., Silhavy, J., et al. (2015). Translational regulation shapes the molecular landscape of complex disease phenotypes. Nat Commun, 6: 6:7200. doi:10.1038/ncomms8200.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002A-3943-D
Abstract
The extent of translational control of gene expression in mammalian tissues remains largely unknown. Here we perform genome-wide RNA sequencing and ribosome profiling in heart and liver tissues to investigate strain-specific translational regulation in the spontaneously hypertensive rat (SHR/Ola). For the most part, transcriptional variation is equally apparent at the translational level and there is limited evidence of translational buffering. Remarkably, we observe hundreds of strain-specific differences in translation, almost doubling the number of differentially expressed genes. The integration of genetic, transcriptional and translational data sets reveals distinct signatures in 3'UTR variation, RNA-binding protein motifs and miRNA expression associated with translational regulation of gene expression. We show that a large number of genes associated with heart and liver traits in human genome-wide association studies are primarily translationally regulated. Capturing interindividual differences in the translated genome will lead to new insights into the genes and regulatory pathways underlying disease phenotypes.