Keeping 'jumping genes' in check could help control some age-related diseases
Most organisms, including humans, have parasitic DNA fragments called "jumping genes" that insert themselves into DNA molecules, disrupting genetic instructions in the process. And that phenomenon can result in age-related diseases such as cancer.
But researchers at the University of Rochester now report that the "jumping genes" in mice become active as the mice age when a multi-function protein stops keeping them in check in order to take on another role.
In a study published today in Nature Communications, Professor of Biology Vera Gorbunova and Assistant Professor of Biology Andrei Seluanov explain that a protein called Sirt6 is needed to keep the jumping genes—technically known as retrotransposons—inactive. That's an entirely different function from the ones scientists had long associated with Sirt6, such as the repairing of broken DNA molecules and regulating metabolism.
"About half of the human genome is made up of retrotransposons," said Gorbunova. "By better understanding why these genomic parasites become active, we hope to better understand and perhaps delay the aging process in humans."
For the most part, retrotransposons remain silent and inactive in organisms' genomes. But once they do become active, these DNA fragments can duplicate themselves and "jump" to new areas of the genome, disrupting the function of another gene by landing in an important part of the gene and changing its DNA sequence information.
But what happens to the Sirt6 proteins that kept the jumping genes inactive in younger cells? The answer lies in the role that Sirt6 plays in repairing DNA damage. Cells accumulate a lot of DNA damage over time that needs to be constantly repaired. As cells get older, Sirt6 becomes busier in taking care of the DNA damage. Gorbunova and Seluanov hypothesized that Sirt6 becomes so preoccupied in repairing DNA damage in older cells that it is no longer available to keep the jumping genes inactive.
To test the theory, the team artificially caused DNA damage in young cells using gamma radiation or the chemical hydrogen peroxide. Once the damage took place, Sirt6 was immediately recruited to the damaged sites of the DNA to do its repair work.
Gorbunova and Seluanov found that the stressed cells—the ones with increased DNA damage—had a higher rate of "jumping gene" activity, when compared to the other cells. Then, when the amount of Sirt6 was artificially increased in the stressed cells, the retrotransposons did not become as readily active, keeping the genome safe.
"This suggests that supplying more Sirt6 protein might protect older cells from aging," said Gorbunova. "The idea would be to increase the Sirt6 pool so that enough proteins are available for both DNA repair and for keeping the retrotransposons inactive."
Peter Iglinski | Eurek Alert!
Toward a 'smart' patch that automatically delivers insulin when needed
18.01.2017 | American Chemical Society
127 at one blow...
18.01.2017 | Stiftung Zoologisches Forschungsmuseum Alexander Koenig, Leibniz-Institut für Biodiversität der Tiere
Yersiniae cause severe intestinal infections. Studies using Yersinia pseudotuberculosis as a model organism aim to elucidate the infection mechanisms of these...
Researchers from the University of Hamburg in Germany, in collaboration with colleagues from the University of Aarhus in Denmark, have synthesized a new superconducting material by growing a few layers of an antiferromagnetic transition-metal chalcogenide on a bismuth-based topological insulator, both being non-superconducting materials.
While superconductivity and magnetism are generally believed to be mutually exclusive, surprisingly, in this new material, superconducting correlations...
Laser-driving of semimetals allows creating novel quasiparticle states within condensed matter systems and switching between different states on ultrafast time scales
Studying properties of fundamental particles in condensed matter systems is a promising approach to quantum field theory. Quasiparticles offer the opportunity...
Among the general public, solar thermal energy is currently associated with dark blue, rectangular collectors on building roofs. Technologies are needed for aesthetically high quality architecture which offer the architect more room for manoeuvre when it comes to low- and plus-energy buildings. With the “ArKol” project, researchers at Fraunhofer ISE together with partners are currently developing two façade collectors for solar thermal energy generation, which permit a high degree of design flexibility: a strip collector for opaque façade sections and a solar thermal blind for transparent sections. The current state of the two developments will be presented at the BAU 2017 trade fair.
As part of the “ArKol – development of architecturally highly integrated façade collectors with heat pipes” project, Fraunhofer ISE together with its partners...
At TU Wien, an alternative for resource intensive formwork for the construction of concrete domes was developed. It is now used in a test dome for the Austrian Federal Railways Infrastructure (ÖBB Infrastruktur).
Concrete shells are efficient structures, but not very resource efficient. The formwork for the construction of concrete domes alone requires a high amount of...
10.01.2017 | Event News
09.01.2017 | Event News
05.01.2017 | Event News
18.01.2017 | Power and Electrical Engineering
18.01.2017 | Materials Sciences
18.01.2017 | Life Sciences