Why the Batteries in Your Body’s Cells Only Come from the Mother and Why It Matters

Some people get a lot from their parents. The color of their eyes, or the shape of their nose, or the crushing loyalty, mysterious in a bad sports team, that must be genetics, because why would anyone choose this pain? (Even with heartache, Go, Habs, Go!) And we inherit some less obvious qualities, including the genetic code that makes everything else we do possible.

Inside each cell—in fact, the cells of most organisms with DNA—is a structure called mitochondria, which produces a substance called adenosine triphosphate (ATP), an important part of the energy we need to stay alive. These small cell batteries have their own type of DNA, which is different from that found in the nuclei of cells. In almost all animals, including humans, that mtDNA is found only in the mother. Why that is has puzzled biologists, but new data could provide an answer, and lead to new treatments for rare diseases.

Although there are cases of people with mtDNA from both parents, it is very rare. In 2016, Ding Xue, a professor of molecular and developmental microbiology at the University of Colorado Boulder set out to find out why. He discovered a complex process that caused my father’s mitochondrial DNA to kill itself.

“It may be embarrassing for the boy to hear, but it’s true,” Xue said in a statement. “Our stuff is so unattractive that evolution has devised many ways to ensure that it is wiped out during production.”

Years ago, Xue began to study what happens in rare cases when that self-destructive sequence is not initiated, and the father’s mitochondria are passed on to the offspring. He chose to try C. elegansa tiny worm with only about 1,000 cells, but still has some human-like tissues, such as the nervous system, intestines, and muscles.

Describes an experiment in a journal Advances in ScienceXue said the worms don’t show any impairment when it comes to their sensory responses, but are affected in other ways, such as showing a reduced ability to remember or learn from bad things. The modified worms were also less efficient in their movement.

None of this is particularly surprising. About 1 in 5,000 people are affected by mitochondrial disease, and symptoms can often include developmental delays, poor vision, muscle weakness, and poor growth. Previous experiments revealed that when mice were modified to have two different mtDNA sequences, there were a number of adverse effects on their metabolism, activity level, and cognition.

What was surprising was that Xue and his colleagues were able to significantly reverse the results, including restoring ATP levels to normal. When they treated the worms with a form of vitamin K2, they found the learning and performance of the worms was “significantly improved.”

Xue’s paper not only explained the advantages of receiving mitochondria from one parent—since adding mitochondrial DNA from a second parent can lead to adverse effects—but also may lay the foundation for future treatments for mitochondrial disorders. He said it is possible that the delay in eliminating paternal mtDNA could be what leads to the disorder in humans. “If you have a problem with ATP it can affect all stages of the human life cycle,” he said.

Worms are delicate creatures, and it is unlikely that giving people with mitochondrial problems vitamin K2 will completely eliminate their conditions. But these disorders can be hereditary, and Xue said, although more research needs to be done, it is possible that giving mothers with a family history of the disease vitamin K2 could reduce the chances of them passing it on to their children.

There is no hope of a cure for the annual disappointment of missing the playoffs. Thank you, father.