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Diseases of the cells’ energy supply can cause a range of serious ailments, but also appear to be connected to aging. More research is required on mitochondrial function to find future treatments. A new study involving researchers at Karolinska Institutet reveals how an important molecule inside the mitochondria affects their function in mice and fruit flies. The study, which is published in Science Advances, adds invaluable information on formerly relatively unexplored protein modifications.
In each cell of the human body is an organ called the mitochondrion, which converts nutrients in our food to energy. Mitochondria are a vital part of the metabolism, and if things go wrong we could create serious diseases.
Mitochondrial dysfunction is the hallmark of a group of rare hereditary disorders but can also be observed in common diseases like diabetes, heart disease, neurodegenerative diseases and the normal aging process.
More research is needed on mitochondria and the way they communicate with the rest of the mobile if scientists are to find new therapeutic approaches to improve mitochondrial function.
Methylation is a chemical modification where a methyl group (CH3) is added to a molecule, thereby potentially affecting its purpose. S-Adenosylmethionine (SAM), also known as AdoMet, is the main methyl group donor within the cell, including inside of mitochondria.
We’re interested in studying this particular molecule since the production of SAM changes in cancer and when we age.”
Anna Wredenberg, Researcher, Department of Medical Biochemistry and Biophysics, Karolinska Institutet
By completely removing SAM in the mitochondria of fruit flies and mice, the researchers have been able to study which processes in the mitochondria are dependent on methylation.
Our study suggests a link between both of these pathways by demonstrating that low SAM levels can affect mitochondrial energy generation.”
The study has identified which of the mitochondrial proteins are methylated and how methylation affects them, and how these modifications might affect cognitive functioning. The researchers also demonstrate the physiological consequences of the lack of such changes.
“Our analysis has provided an indication that some alterations can be modulated by diet, but we need to keep on examining if we can alter the pathological process for the better,” says Anna Wredenberg. “So far we have only looked at protein changes, but other molecules may also be modified by intra-mitochondrial SAM. We must study these modifications to get a better understanding of the role it plays.”
Karolinska Institutet
Schober, F.A., et al. (2021) The one-carbon pool controls mitochondrial energy metabolism via complex I and iron-sulfur clusters. Science Advances. doi.org/10.1126/sciadv.abf0717.
