Biologically speaking, we take more from our mothers than from our fathers. Apart from important medical implications, this information could help you make a point if your mom shouts at you: “You’re just like your father!”
While males and females contribute equal amounts to the genetic material of offspring, in most animals the mitochondria – where chemical energy is released in cells – come exclusively from the maternal lineage. The fact that sperm mitochondria are not passed on has been a longstanding mystery, but now scientists might have uncovered why.
An international team of researchers has observed that if the paternal mitochondria remain after fertilization, there’s a lower survival chance for the embryo. The discovery is published in the journal Science.
The team used electron microscopy and tomography to look at the fertilization of Caenorhabditis elegans, a type of roundworm. They were trying to see when exactly autophagosomes, cellular structures that can break down useless part of the cells, begin to attack the sperm mitochondria. Surprisingly, the team discovered that the paternal mitochondria were already partly destroyed when that happened.
The finding suggests an internal origin for a self-destruct button. When the researchers probed further, they discovered that paternal mitochondrial DNA has a gene, called cps-6, that is activated at fertilization. Cps-6 activates an enzyme that first digests the interior membrane and subsequently destroys the mitochondrial DNA.
To test the importance of this gene, the team engineered C. elegans sperm so that the gene would activate at later stages. They discovered that this change increased the mortality rate of the offspring by five to seven times.
The fact that the embryos might die if the paternal mitochondria survive tells us that embryos that keep them for longer have an evolutionary disadvantage.
Although this study was performed on roundworms, cps-6 has an equivalent gene in humans – endonuclease G – that has already been implicated in cancer, aging, and neurodegenerative diseases.