Disruptions in the supply of energy to cells can cause a number of serious diseases, but they also appear to be linked to aging. More research on mitochondrial function is needed to find future treatments. A new study with researchers from the Karolinska Institutet shows how an important molecule in the mitochondria affects their function in mice and fruit flies. The study that will be published in Advances in scienceadds valuable knowledge of previously relatively unexplored protein modifications.
Every cell in the body has an organ called the mitochondrion that converts nutrients in our food into energy. Mitochondria are an essential part of metabolism and when things go wrong we can develop serious diseases.
Mitochondrial dysfunction is the hallmark of a group of rare genetic disorders, but it can also be seen in common diseases such as diabetes, heart disease, neurodegenerative diseases, and the normal aging process.
More research on mitochondria and how they communicate with the rest of the cell is needed if scientists are to find new therapeutic approaches to improve mitochondrial function.
Researchers at the Karolinska Institutet, the Max Planck Institute for Biology of Aging in Cologne and the University of California in San Diego have now investigated how the methylation of proteins affects various mitochondrial processes.
Methylation is a chemical modification in which a methyl group (CH3) is added to a molecule, potentially affecting its function. S-adenosylmethionine (SAM), also known as AdoMet, is the major methyl group donor within the cell, including within the mitochondria.
"We are interested in studying this particular molecule because SAM production changes in cancer and as we get older," says Anna Wredenberg, researcher at the Institute of Medical Biochemistry and Biophysics at the Karolinska Institutet.
By completely removing SAM from the mitochondria of fruit flies and mice, the researchers were able to study which processes in the mitochondria depend on methylation.
"Previous studies have shown that both SAM and cellular energy levels decrease with aging. Our study suggests a link between these two pathways by showing that low SAM levels can affect mitochondrial energy production."
The study found which of the mitochondrial proteins are methylated and how methylation affects them and how these modifications could affect mitochondrial function. The researchers also show the physiological consequences of the lack of such changes. However, some questions still need to be answered.
"Our study showed that some changes can be modulated by diet, but we need to further investigate whether we can change the pathological process for the better," says Anna Wredenberg. "So far we have only looked at protein changes, but other molecules can also be modified by intra-mitochondrial SAM. We need to study these modifications to get a better understanding of the role they play."
The study was funded by the Swedish Research Council, the European Research Council, the Knut and Alice Wallenberg Foundation, the Max Planck Society and the Ragnar Söderberg Foundation. No conflicts of interest were reported.
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