Last updated March 15, 2018 at 10:43 am
RNA holds the key to Haloferax volcanii’s ability to cope with extreme heat.
The Atacama Desert’s Volcanic landscape may be beautiful, but it is one of the harshest environments on Earth. Credit: iStock
The discovery of the mechanism by which a species of extremophile deals with the consequences of heat, aridity and hyper-salinity reveals a connection with how the human body responds to cardiovascular and neurodegenerative disease threats.
Research led by biologist Diego Rivera Gelsinger of Johns Hopkins University in Maryland in the US shows that the extremophile – a species of archaean called Haloferax volcanii – controls the threat of destructive free radicals by exploiting exactly the same genetic pathway used by bacteria and eukaryotes, the nucleic cells that comprise all complex life.
The finding, published in the Journal of Bacteriology, suggests that the survival mechanism is extremely ancient, and that its relative efficiency across species is governed by regulation, not anatomy.
Haloferax volcanii lives in rock pores in the Atacama Desert in Chile and endures one of the harshest environments on the planet. The high amounts of solar radiation and salt to which the organisms are exposed should induce equally high levels of oxidative stress – the process by which oxygen catalyses the production of DNA-damaging molecules called free radicals.
Under extreme stress
For any other organism, conditions in the archaean microhabitat would result in death, very quickly, yet H. volcanii, Gelsinger and colleagues report, is “an order of magnitude more resistant to oxidative stress” than anything else on Earth.
Discovering just how it achieves this feat was the aim of the team’s research. And the answer, it seems, lies in the archaean’s ribonucleic acid, or RNA.
RNA is best known as a “messenger”, a substance within the cell that takes blueprint instructions from DNA and then uses them to create essential proteins.
By analysing what happens when H. volcanii is placed under stress – in this case by being exposed to hydrogen peroxide – Gelsinger and colleagues noticed something unusual. As well as messenger-RNA (mRNA), also present were significant quantities of RNA of a different type – known as non-coding RNA.
These segments do not create proteins, but the researchers discovered that they played an important protective role – by hampering the function of the messenger-RNA.
Disrupting the disruptors
“My findings strongly suggest that the [noncoding RNA] actually causes the messenger RNA to degrade and be cut up,” explains Gelsinger.
By doing so, they essentially prevented the production of the proteins that give rise to oxidative stress. The research also showed that the non-coding RNA accounted for as much as 30% of all the RNA present, and attacked multiple targets. Among these were transposons – DNA segments that when under stress flit around inside the cell potentially doing a lot of damage.
In effect, the non-coding RNA was disrupting the disruptors.
“What we found is that a lot of these noncoding RNAs are causing the degradation of those transposons, so they are essentially silencing them,” says Gelsinger.
These segments of RNA, the researchers state, play a major role in reducing the effects of oxidative stress in the Archaean, permitting it to thrive in an environment that would be lethal to most other lifeforms.
The research, the scientists conclude, “demonstrates that common principles for the response to a major cellular stress” exist in archaea, bacteria and eukaryotes, the three major domains of life.
Teasing out the similarities and differences in the way species regulate the process could one day provide targets for a wide range of human diseases in which oxidative stress is known to play a role.
