A building block for liver fitness in old age Researchers discover cellular protection against epigenetic changes

13.09.2022 | Dr. Peter Tessarz

The structure of the liver changes with age. Shown here is a histology image of young (left) and old (right) liver cells. © Max Planck Institute for Biology of Ageing, 2022

Researchers discover cellular protection against epigenetic changes

The liver can regenerate even in old age and remains surprisingly fit, even though the chromatin in its cells undergoes major remodeling due to epigenetic changes, as researchers from the Max Planck Institute for Biology of Ageing in Cologne have now discovered. One possible reason why the transformation has minor consequences could be a mechanism that the researchers now describe in the journal Molecular Systems Biology.

Changes in epigenetics are considered to be a cause of ageing processes. Epigenetics describes changes in genetic information that do not alter the sequence of the genes themselves, but influence their activity. Among other things, this can be regulated by the accessibility of proteins to DNA as part of chromatin. In this study, the researchers observed in liver cells that the DNA of liver cells becomes much less packaged with age. This makes the DNA more accessible to produce the messenger molecule RNA. "If the DNA is readily accessible, we should also see greater amounts of RNA made. But that was not the case at all," says Peter Tessarz, head of the study at the Max Planck Institute for Biology of Ageing and principal investigator at CECAD Cluster of Excellence on Aging Research at the University of Cologne.

Shorter break at the DNA

The researchers already have a possible explanation for this. They found that RNA polymerase, a protein that binds to DNA and then produces RNA, falls off from the DNA more quickly in aged liver cells than in young cells. This reduced stability means that, despite increased accessibility to DNA, there is no net increase in RNA production, maintaining the balance within the cell.

"We think we have discovered a new pathway in cells that compensates for age-dependent epigenetic changes. This could be one reason for the liver's ability to keep functioning for so long. Whether a similar mechanism counteracts epigenetic changes in other tissues remains to be explored in the future. There, however, we also observe completely different epigenetic changes during ageing," says Tessarz.

The research for this study was conducted at the Max Planck Institute for Biology of Ageing and was funded by the CECAD Cluster of Excellence for Aging Research

 

Press picture:

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Caption: The structure of the liver changes with age. Shown here is a histology image of young (left) and old (right) liver cells.

© Max Planck Institute for Biology of Ageing, 2022

Original publication:

Mihaela Bozukova, Chrysa Nikopoulou, Niklas Kleinenkuhnen,Dora Grbavac, Katrin Goetsch, Peter Tessarz

Aging is associated with increased chromatin accessibility and reduced polymerase pausing in liver

Molecular Systems Biology, September 9th, 2022

https://www.embopress.org/doi/full/10.15252/msb.202211002

 

Contact:

Corresponding author: Dr. Peter Tessarz

Max Planck Institute for Biology of Ageing, Cologne

Tel.: +49 (0)221 379 70 680
E-mail: peter.tessarz[at]age.mpg.de

 

Press and public relations: Dr. Maren Berghoff

Max Planck Institute for Biology of Ageing, Cologne

Tel.: +49 (0)221 379 70 207

E-mail: maren.berghoff[at]age.mpg.de 

About the Max Planck Institute for Biology of Ageing

The Max Planck Institute for Biology of Ageing investigates the natural ageing process with the long-term goal to pave the way towards increasing health during ageing in humans. It is an institute within the Max Planck Society, which is one of Germany’s most successful research organisation. Since its foundation in 2008 the institute is an integral part of the DFG-funded Cluster of Excellence in Ageing Research CECAD at the University of Cologne.

www.age.mpg.de