A team of researchers led by scientists at the University of Nottingham, England, proposed an explanation for the fact that transposons, the so-called jumping genes that can be found in most living organisms, don’t kill their hosts.

Transposons are genetic elements that can move within the DNA of an organism, typically leaving copies of themselves in the original location. A variant is that of retrotransposons, that move using RNA as an intermediary. Transposons were discovered by biologist Barbara McClintock in the ’40s doing experiments with maize plants (photo ©Asbestos) finding that their caryopses can have different colors due to the activity of transposons. For her discoveries, she received the Nobel Prize for Medicine or Physiology in 1983.

Our genetic knowledge have grown tremendously in the following decades but the exact role of transposons is still under discussion. They’re considered almost viral elements that can cause disease but may also be evolutionary factors for the mutations they cause in the DNA to so many different organisms.

An extreme example of the activity of transposons is the Norway spruce (Picea abies), commonly known as the European spruce, whose DNA contains over 20 billion bases. For comparison, the DNA of human beings has about 3 billion bases. This is due to the fact that this species of spruce has a quantity of transposons much greater than any other species examined so far. Recently, an international team finished mapping the DNA of this species of spruce among other things to try to understand the reasons for this anomalous growth.

A mystery remained at the base of the activity of transposons: why don’t they replicate exponentially until they kill their hosts? According to Ronald Chalmers, a Professor of Molecular and Cellular Biology at the University of Nottingham, who participated in the research on this issue, the explanation is that a parasite is successful when it manages somehow to live in harmony with its host without killing it.

Professor Ronald Chalmers and his colleagues examined transposons existing in human DNA and used computer models to try to understand the biochemical mechanisms used by those jumping genes to regulate their growth. The result was the discovery that, once they reached a certain number of copies, transposons begin to interfere with each other stopping the process that lead to their replication.

This could be a significant step forward in genetic research because it may help us to better understand the mechanisms of certain diseases and evolution with possible repercussions in the field of genetic engineering.

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