Why We Inherit Mitochondria Only From Mothers – Neuroscience News

Summary: A recent study reveals why many animals, including humans, inherit mitochondrial DNA only from their mothers, suggesting that retaining paternal mitochondria may impair development. first and health. In worms, when paternal mitochondria persist, it disrupts ATP production, which affects the nervous system, behavior and reproductive health of the offspring.

This study suggests that paternal mitochondrial clearance issues may play a role in certain mitochondrial disorders. Interestingly, treating the affected worms with vitamin K2 restored ATP levels and improved their function, suggesting a new way to control mitochondrial diseases in humans.

Important Points

• Paternal mitochondria can disrupt ATP production and harm health if stored.
• Vitamin K2 restored ATP levels in worms with impaired mitochondrial function.
• Study findings may inform future treatments for mitochondrial disorders.

Source: University of Colorado

It’s one of the basic lessons of biology: We get our DNA from our mother and father.

But one exception has puzzled scientists for decades: Most animals, including humans, inherit the DNA in their mitochondria — the cell’s powerhouses — only from their mothers. , with all traces of their father’s mitochondrial genome destroyed once the sperm meets the egg.

A new University of Colorado Boulder study published Oct. 4 in the newspaper Advances in Science sheds new light on why this happens, showing that when the process fails, and the father’s mitochondria enter the developing baby, it can lead to problems neurodegenerative, behavioral and reproductive disorders in adults.

The study, carried out in worms, provides new information about what can drive mitochondrial problems, which interfere with the body’s ability to produce energy and affect 1 in 5,000 people in total. It also introduces a new way to prevent or treat them – a simple vitamin known as Vitamin K2.

“These findings provide important new insights into why paternal mitochondria must be rapidly removed during early development,” said senior author Ding Xue, a professor in the Department of Molecular, Cellular and Developmental Biology (MCDB) at the University of Colorado Boulder.

They also offer new hope for the treatment of human diseases that may be caused when this process is compromised.”

When cell phone batteries run down

Often described as cellular batteries, mitochondria produce adenosine triphosphate (ATP), the energy that drives almost all cellular activity.

Mitochondria have their own unique DNA, which is usually passed down only from their mother.

In 2016, Xue published one of the first papers to describe how paternal mitochondria are eliminated – in a multifaceted, self-destructive process known as paternal mitochondria elimination (PME ),” an activity written about worms, rats and. people alike.

“It might be humiliating for a guy to hear, but it’s true,” Xue joked. “Our stuff is so unattractive that evolution has devised many ways to make sure it gets cleaned up during reproduction.”

Some theorize that after battling millions of other sperm to penetrate the egg, the sperm’s mitochondria become exhausted and the genes become damaged in ways that could be dangerous to evolution if they are passed on to future generations.

Xue and his team set out to find out what happens when the father’s mitochondria don’t destroy themselves.

They learned C. elegans, a translucent worm that has only 1,000 cells but develops a nervous system, intestines, muscles and other cells similar to humans.

The team was unable to completely stop PME in worms – proof of how robust this evolution is. But they were able to delay it for about 10 hours. When they did that in fertilized eggs, it led to a significant reduction in ATP. If the worms were to survive at all, they were not well-informed, have altered function and had difficulty reproducing.

When the researchers treated the worms with a form of vitamin K2 known as MK-4 (best known as a bone health supplement) it restored ATP levels to normal in the embryos and improved memory. , activity and reproduction in adult worms.

Hope for poorly understood diseases

The authors note that there are only a few reported cases where paternal mitochondrial DNA could have been found in adults. One paper describes a 28-year-old man who had difficulty breathing, weak muscles and could not tolerate exercise. Another documents 17 members of three unrelated multigenerational families who had fatigue, muscle pain, speech delay and neurological symptoms.

More research is needed in larger animals, but Xue suspects that in some cases, such as worms, a delay in PME could cause human diseases that are difficult to detect.

“If you have a problem with ATP it can affect every stage of the human life cycle,” he said.

Xue envisions a day when some families with a history of mitochondrial disorders take vitamin K2 during pregnancy as a preventative measure. The study, and ongoing lab research, may also lead to new ways to diagnose or treat mitochondrial diseases.

“There are many diseases that are not well understood. No one really knows what’s going on. This research provides clues,” Xue said.

About this research issues of mitochondria and genetics

Author: Lisa Marshall
Source: University of Colorado
Contact: Lisa Marshall – University of Colorado
Image: Image credited to Neuroscience News

Basic research: Open access.
“Delayed embryonic balance of paternal mitochondrial elimination disrupts mating and cognition and alters behavior in large animals” by Ding Xue et al. Advances in Science

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Summary

Embryonic delay in paternal mitochondrial elimination disrupts mating and cognition and alters behavior in large animals.

The rapid elimination of paternal mitochondria after conception is a conserved phenomenon in many animals, but its physiological significance remains unclear.

We find a slight delay in paternal mitochondrial elimination (PME) in the Caenorhabditis elegans the embryos interfere with the mating and cognition of large animals and change their movement patterns.

Delayed PME causes a decrease in the level of adenosine triphosphate (ATP) in the early oocytes, which leads to the inactivation of the large animal’s energy-sensitive pathway mediated by adenosine monophosphate (AMP) – activated protein kinase, AAK-2, and box fork. group O (FOXO) transcription factor, DAF-16.

Treatment of PME-induced animals with MK-4, a form of vitamin K₂ which can improve mitochondrial ATP production, restore ATP levels to original levels, and rescue the body’s weakness in large animals.

Our results suggest that a moderate delay in PME during embryonic development negatively affects important physiological functions in adults, which may be harmful.

These findings provide clear explanations for the need to remove paternal mitochondria early during fetal development.