Paternal mitochondria harm offspring | Science and life

Lingering in the embryo, the paternal mitochondria deprive it of energy.

When we say that children receive two copies of genes, from their mother and from their father, we mean those genes that are located on chromosomes, that is, in nuclear DNA. During fertilization, paternal chromosomes are added to the maternal chromosomes in the egg, which are brought by the sperm. The gene variants on the maternal and paternal chromosomes may be the same, or they may be different – one way or another, in organisms with sexual reproduction, the parental genomes are combined.

The inner membrane of mitochondria forms folds-cristae, increasing its area. The inner membrane contains enzymes of the electron transport respiratory chain and ATP synthesis. (Illustration: SkieTheAce / Pixabay.com)

But in cells, in addition to nuclear DNA, there is mitochondrial DNA. Mitochondria are involved in a large and very complex block of biochemical reactions that provide the cell with energy in the form of ATP molecules. Some proteins that are needed for energy reactions are encoded in mitochondrial DNA. And mitochondria are capable of synthesizing these proteins themselves; Although they do not completely provide themselves with everything they need, they also need proteins encoded in nuclear DNA.

Mitochondria are found in all cells, including germ cells. But during fertilization, the paternal mitochondria are destroyed, so the mitochondrial genome is inherited exclusively through the maternal line. The mechanisms of destruction of paternal mitochondria are being actively studied, and now we know that they are carried out by the waste disposal systems of the egg, destroying unnecessary proteins and organelles. In addition, in the paternal mitochondria themselves, after fertilization, a self-destruction mechanism is activated, associated with a special enzyme that specifically breaks down mitochondrial DNA. Somewhat less is known about why they should be destroyed in the first place.

Ding Xue (Ding Xue) and his colleagues from University of Colorado Boulder experimented with roundworm embryos Caenorhabditis elegans. They tried to preserve the paternal mitochondria in the worm eggs by suppressing the activity of the gene for the above-mentioned enzyme that breaks down mitochondrial DNA. It was never possible to save them – the mitochondria were destroyed by other means, which suggests that it is very important for the cell that they are not left. However, the paternal mitochondria managed to extend their lifetime by about ten hours (the larva is born from the egg at the fifteenth hour after the start of embryogenesis).

In an article in Science Advances it is said that in embryos with delayed paternal mitochondria, the level of ATP, the very molecule in which energy is stored in a form convenient for the cell, was reduced. The lack of ATP affected some signaling pathways operating in the embryo. Apparently, as a result, such embryos died more often, and those that were born showed problems with memory, learning and mating behavior in adulthood, and they had some other anomalies that distinguish them from ordinary worms. None of this happened when fetuses were given vitamin K.2
– with it, the level of ATP in the germ cells increased to the normal level, and in adult worms everything was fine with memory and other things.

It would seem that paternal mitochondria should create an excess of energy, but here everything turned out the other way around. Most likely, this is due to the fact that the mitochondria of male sperm enter the egg already in a very tattered form: their membranes are severely damaged, which lose the potential difference and begin to freely allow various molecules to pass through them. An important part of the energy reactions take place on the membranes of mitochondria, and if they deteriorate, you cannot count on excess energy. In addition, defective mitochondria affect the cellular environment around them, and the effect is bad. But this is only one explanation for why the egg tries to get rid of the father’s mitochondria.

There are other hypotheses here – for example, that maternal mitochondria have already “worked together” with nuclear DNA, and new paternal ones introduce some discord into the established cooperation. (Although some researchers believe that the disagreement between the mitochondrial and nuclear genomes is to the cell’s advantage.) In any case, judging by the effect that the father’s mitochondria have on the offspring, they really are worth getting rid of. Similar experiments have been carried out before, but now it has been possible to trace the negative impact of paternal mitochondria not only on eggs and embryos, but also on adult offspring.

Source: www.nkj.ru