Some people get a lot of things from their parents. The color of their eyes, or the shape of their nose, or their overwhelming, inexplicable loyalty to a terrible sports team must be genetic, so why would anyone choose this torment? (Even with the heartache, go, Hubs, go!) We also inherit some less obvious traits, including the genetic coding that makes everything we do possible.
Inside each of our cells – in fact the cells of most organisms that contain DNA – is a structure called mitochondria, which produces a substance called adenosine triphosphate (ATP), which is vital for the energy we need to survive. These tiny cell batteries contain their own form of DNA, which is different from that found in the nucleus of cells. In almost all animals, including humans, this mitochondrial DNA is inherited only from mothers. Biologists have puzzled over why this happens, but new data could provide an answer, and lead to new treatments for some rare disorders.
While there are cases of humans having mtDNA from both parents, this is extremely rare. In 2016, Ding Xue, a professor of molecular and developmental microbiology at the University of Colorado Boulder, set out to find out why. Discover a complex process that leads to the destruction of parental mitochondrial DNA itself.
“It may be insulting for a man to hear, but it is true,” Xue said in a message. statement. “Our stuff is so undesirable that evolution designed multiple mechanisms to make sure it gets removed during reproduction.”
In the intervening years, Xue set out to find out what happens in the rare cases in which the self-destruct sequence does not initiate, and parental mitochondria are passed on to offspring. He chose to experiment C. elegansa small roundworm consisting of only about 1,000 cells, but still has some tissues in common with humans, such as the nervous system, intestines, and muscles.
a description an experience In the magazine Advancement of scienceXue said the worms showed no defects when it came to their sensory responses, but were affected in other ways, such as showing a reduced ability to remember or learn from negative stimuli. The mutant worms were also less active in their movements.
None of this is particularly surprising. About one in 5,000 people are affected by mitochondrial disease, and symptoms can often include delayed growth, cognitive impairment, muscle weakness, and poor growth. Previous experiments revealed that when mice were modified to have two different mtDNA sequences, there were a number of negative effects on metabolism, activity level, and cognition.
What was surprising was that Xue and his colleagues were able to significantly reverse the effects, including returning ATP levels to normal. When they treated the worms with a type of vitamin K2, they found that the worms’ learning and memory performance “significantly improved.”
Xue’s paper not only explained the benefits of inheriting mitochondria from one parent—as adding mitochondrial DNA from a second parent can lead to harmful effects—but it may also have laid the foundation for future treatments for mitochondrial disorders. He said it is possible that a delay in eliminating paternal mitochondrial DNA is what leads to the disorders that occur in humans. “If you have a problem with ATP, it can affect every stage of the human life cycle,” he said.
Roundworms are simple creatures, and it is unlikely that simply giving humans with mitochondrial disorders vitamin K2 will completely cure their condition. But the disorders can be hereditary, and Xue said that although more research is needed, it is possible that giving vitamin K2 to mothers with a family history of the disease could reduce the chances of passing it on to their children.
There is still no cure for the annual disappointment of missing the playoffs. Thanks, dad.
“Devoted student. Bacon advocate. Beer scholar. Troublemaker. Falls down a lot. Typical coffee enthusiast.”