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Epigenetic control of cardiogenesis
Date:1/29/2013

This press release is available in German.

Many different tissues and organs form from pluripotent stem cells during embryonic development. To date it had been known that these processes are controlled by transcription factors for specific tissues. Scientists from the Max Planck Institute for Molecular Genetics in Berlin, in collaboration with colleagues at MIT and the Broad Institute in Boston, have now been able to demonstrate that RNA molecules, which do not act as templates for protein synthesis, participate in these processes as well. The scientists knocked down a gene for long non-coding RNA molecules (lncRNA) and thereby disrupted the development of the heart to an extent that was lethal to the embryos. Genesis of the ventral body wall was also impaired. It became apparent that the lncRNA participates in controlling transcription factors that themselves are responsible for controlling tissue- and organogenesis. The lncRNA itself thus acts as a modulating factor in these processes.

RNA molecules more than 300 nucleotides long and not exhibiting any protein-coding read frames are denoted as long non-coding RNA. They are known to interact with histone-modifying protein complexes that control the activation state of genes (activatable, active, or repressed), as well as influencing the level of their activity. This occurs, for example, through the transfer of methyl groups to histones, the DNA-packaging proteins. Modifications to the histones such as these can be copied during cell division and thus promulgate the activation state of genes from cell to cell across several stages of differentiation.

Max Planck scientists led by Bernhard Herrmann have proven for the first time that lncRNAs may also be indispensable for embryonic development. This was previously known primarily for transcription factors. They discovered an lncRNA, termed
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Contact: Bernhard G. Herrmann
herrmann@molgen.mpg.de
49-308-413-1409
Max-Planck-Gesellschaft
Source:Eurekalert  

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Epigenetic control of cardiogenesis
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