News Release

'Cheater mitochondria' may profit from cellular stress coping mechanisms

Interactions between evolutionary pressures at the cellular and environmental level may enable cheating mitochondria to persist despite potential harm to individual organisms

Peer-Reviewed Publication

eLife

Cheating mitochondria may take advantage of cellular mechanisms for coping with food scarcity in a simple worm to persist, even though this can reduce the worm's wellbeing.

These findings, published today in eLife, may help shed light on the evolution of cheating and cooperative behaviours within different organisms.

Mitochondria are energy-producing units within cells that likely evolved from bacteria. They have their own DNA, take in resources from cells, and in exchange provide the cell with energy. But some so-called 'cheater mitochondria' have harmful DNA mutations that may reduce their energy output and harm the organism. Why these cheater mitochondria persist despite their harm to the larger organism is not currently clear.

"Cooperation and cheating are widespread evolutionary strategies," says lead author Bryan Gitschlag, a PhD student at the Department of Biological Sciences, Vanderbilt University, Nashville, Tennessee. "While cheating confers an advantage to individual entities within a group, competition between groups favours cooperation."

Gitschlag and his colleagues studied the roundworm Caenorhabiditis elegans to see how competing evolutionary pressures within its cells and in its environment might enable the cheater mitochondria to persist.

They measured the levels of cheater and typical mitochondria in the worm's cells. They found that, within the cells, a protein called DAF-16, which helps cells to survive stress, is necessary for cheater mitochondria to multiply. When the worms face food shortages, cheater mitochondria become more harmful to their hosts, but only in those lacking DAF-16. "This shows that food scarcity can strengthen evolutionary selection against worms carrying cheater mitochondria, but DAF-16 protects them from it," Gitschlag explains.

The results suggest that competing selection pressures within an organism and in its environment may shed light on why selfishness and cooperation often exist side-by-side among populations.

"The ability to cope with scarcity can promote group-level tolerance to cheating, inadvertently prolonging cheater persistence," says senior author Maulik Patel, Assistant Professor of Biological Sciences at Vanderbilt University.

"As selfish mitochondrial genomes are implicated in numerous disorders, and cheating is a widespread evolutionary strategy, it will be interesting to apply our methods to study a broader collection of cheating variants and host species. This could allow us to better understand the development of mitochondrial disorders or the evolutionary principles underlying cooperation and cheating," Patel concludes.

###

Reference

The paper 'Nutrient status shapes selfish mitochondrial genome dynamics across different levels of selection' can be freely accessed online at https://doi.org/10.7554/eLife.56686. Contents, including text, figures and data, are free to reuse under a CC BY 4.0 license.

Media contact

Emily Packer, Media Relations Manager
eLife
e.packer@elifesciences.org
01223 855373

About eLife

eLife is a non-profit organisation created by funders and led by researchers. Our mission is to accelerate discovery by operating a platform for research communication that encourages and recognises the most responsible behaviours. We work across three major areas: publishing, technology and research culture. We aim to publish work of the highest standards and importance in all areas of biology and medicine, including Evolutionary Biology and Genetics and Genomics, while exploring creative new ways to improve how research is assessed and published. We also invest in open-source technology innovation to modernise the infrastructure for science publishing and improve online tools for sharing, using and interacting with new results. eLife receives financial support and strategic guidance from the Howard Hughes Medical Institute, the Knut and Alice Wallenberg Foundation, the Max Planck Society and Wellcome. Learn more at https://elifesciences.org/about.

To read the latest Evolutionary Biology research published in eLife, visit https://elifesciences.org/subjects/evolutionary-biology.

And for the latest in Genetics and Genomics, see https://elifesciences.org/subjects/genetics-genomics.


Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.