Mitochondria fling DNA into our brain cells, making us age faster

As direct descendants of ancient bacteria that invaded early eukaryotic cells, mitochondria have always been somewhat alien, possessing their own unique genetic material and evolutionary history.

Recent research has shown that mitochondria in our brain cells often send their DNA into the nucleus, where it integrates into the cell’s chromosomes, blurring the distinction between mitochondrial and nuclear genetic material.

Link to early mortality

The team behind this discovery was led by Martin Picard from Columbia University and Ryan Mills from the University of Michigan. The study shows that mitochondrial DNA insertions could be linked to early mortality.

“We used to think that the transfer of DNA from mitochondria to the human genome was a rare occurrence,” said Picard, highlighting the unexpected frequency of this phenomenon.

Mitochondrial DNA acts like a virus

Mitochondria are unique among cell organelles because they carry their own circular DNA, a remnant of their bacterial ancestry.

This DNA behaves in a way that is surprisingly similar to a virus, capable of jumping into human chromosomes and integrating itself into the host genome.

The viral-like behavior of mitochondrial DNA, as described by Ryan Mills, is similar to the action of retrotransposons, also known as “jumping genes.” These are mobile genetic elements that can move around and insert themselves into different parts of the human genome.

These DNA insertions, known as nuclear-mitochondrial segments (NUMTs), have been silently accumulating in our DNA over millions of years, leaving a lasting genetic footprint that connects our evolutionary past to our present-day biology.

“As a result, all of us are walking around with hundreds of vestigial, mostly benign, mitochondrial DNA segments in our chromosomes that we inherited from our ancestors,” explained Mills.

Segments of mitochondria in the brain

Recent findings demonstrate that NUMTs are not just relics of the distant past; they are actively being created today.

The ongoing integration of mitochondrial DNA into nuclear chromosomes is particularly prevalent in the brain, with the prefrontal cortex showing the highest concentration of these insertions.

This suggests that certain regions of the brain may be more susceptible to NUMT formation, which could potentially influence cognitive functions and overall neurological health, highlighting the significance of NUMTs in brain aging and disease.

Mitochondria influence aging and lifespan

“Jumping mitochondrial DNA is not something that only happened in the distant past,” noted Kalpita Karan, a postdoctoral researcher in Picard’s lab.

The study, using samples from the ROSMAP aging study, indicates that individuals with more NUMTs in their brains tend to have a shorter lifespan.

“This suggests for the first time that NUMTs may have functional consequences and possibly influence lifespan,” said Picard.

How stress infects the nuclear genome

Further research involving cultured human skin cells revealed that stress can accelerate the accumulation of NUMTs.

“Stress makes mitochondria more likely to release pieces of their DNA, and these pieces can then ‘infect’ the nuclear genome,” said Weichen Zhou, a research investigator from Mills’ lab.

This finding opens a new avenue for understanding the mechanisms by which stress impacts cellular biology and accelerates the aging process, further linking mitochondrial health to overall well-being.

Mitochondrial DNA and health risks

The study sheds light on the multifaceted role of mitochondria, not just as energy providers but also as key players in cellular signaling and genetic stability.

“Mitochondria are cellular processors and a mighty signaling platform,” said Picard. Their ability to alter nuclear DNA sequences may have significant implications for aging and longevity, adding a new layer to our understanding of these ancient organelles.

The discovery that mitochondrial DNA can integrate into the nuclear genome multiple times during a person’s lifetime raises important questions about its impact on health.

These NUMT insertions might not always be benign. Depending on where they integrate, they could disrupt crucial genes or regulatory regions, potentially leading to various health issues.

Potential for therapeutic advances

Understanding how NUMTs contribute to disease processes could lead to new diagnostic markers or therapeutic targets.

For example, monitoring the presence and frequency of NUMTs in brain cells might help identify individuals at higher risk for certain neurological conditions.

Furthermore, developing strategies to minimize or repair the harmful integration of mitochondrial DNA could provide new avenues for treating or preventing age-related diseases.

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