Mitochondria can sneak DNA into the nuclei of brain cells

Scientists have found DNA contained within the nucleus of brain cells, where it shouldn’t be. Bits of genes that generally reside in mitochondria insert themselves at all of a sudden high rates into brain cells’ nuclear genomes.

What’s more, these insertions would per chance be associated with life span. In a study of nearly 1,200 older adults, the more mitochondrial insertions a non-public had, the younger they died, mitochondrial biologist Martin Picard of Columbia University and colleagues report August 22 in PLOS Biology. The finding implies that researchers may someday measure or target the insertions to take hold of and treat certain age-related conditions or conditions characterized by malfunctioning mitochondria.

An unexpected presence contained within the brain

Mitochondria are well-referred to as energy producers within a cell. But that’s now not their best job. There are “15 or 20 different things that mitochondria can do to change how the cell behaves,” Picard says. One in all those processes is shipping their own DNA to the nucleus of cells, he says, which is then integrated into the nuclear genome. Researchers have observed this process, referred to as numtogenesis, in human cancer cells and reproductive cells. However it surely had now not been observed in human brain tissue sooner than.

So Picard’s team made use of banked postmortem tissue — blood and brain cells — from 1,187 older adults. The researchers quantified the choice of mitochondrial DNA insertions in tissue across brain areas, including the dorsolateral prefrontal cortex, or DLPFC, and the cerebellum. The DLPFC is involved in decision making and executive function, and the cerebellum controls movement and coordination.

Mitochondrial insertions and our health

The usage of skin cells collected from living patients, the team sought to study how cellular aging influenced the choice of mitochondrial insertions. On average, the cells accumulated one mitochondrial insertion every 13 days in lab dishes.

Mitochondrial insertions increased even more less than stressors like genetic mutations or drug treatments. The medication dexamethasone, which induces mitochondrial dysfunction, and oligomycin, which inhibits a mitochondrial enzyme, a bit increased the rate of numtogenesis. Skin cells from patients deficient for the gene SURF1, which is associated with a severe mitochondrial disease referred to as Leigh syndrome (SN: 12/14/16), accumulated insertions almost 5 times as fast as regulate cells.

To Picard, which means numtogenesis would per chance be a strategy that mitochondrial dysfunction ends in pathology and contributes to conditions that cause premature death, like Leigh syndrome.

Overall, the study provides evidence that numtogenesis can happen in organs a dead ringer for the brain, and would per chance even occur more in some body areas or tissues than in others, says Anabelle Decottignies, a molecular biologist on the University of Louvain in Belgium who became now not involved contained within the work. But the prospective health consequences of these insertions are still unclear. “What we still don’t know is whether or not [the insertions] hurt someway the tissues,” Decottignies says.

Miria Ricchetti, a molecular biologist on the Pasteur Institute in Paris who became now not involved with the study, says that it'll be essential to study where contained within the nuclear genome the mitochondria DNA is sneaking into to take hold of how it should per chance be affecting the cell.

Future studies also should unravel how these mitochondrial insertions can cause disease, Picard says. If that’s established, he sees the insertions as a potential thanks to measure health. “My hunch at present is that the more healthy you could be, the less [insertions] you’re going to increase,” he says.