Biologically, male and female contribute equal amounts to the genetic material of offspring. Our mitochondrial DNA accounts for a small portion of our total DNA. It contains just 37 of the 20,000 to 25,000 protein-coding genes in our body. But it is notably distinct from DNA in the nucleus.
Unlike nuclear DNA, which comes from both parents, mitochondrial DNA comes only from the mother. Inheritance of the mitochondria and plastids is a non-nuclear inheritance. They are inherited from the mother only and the Y chromosome is inherited from the father only.
Thus, these chromosomes are helpful in determining the lineages and the mutation rates (for example the mutation rates of certain maternally inherited genes and disease occurrence, etc.). No parental mitochondrial get passed on to the children. The researcher has observed that if the paternal mitochondria remain after fertilization, there is lower survival chance for the embryo.
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. The gene cps-6 encodes a mitochondrial DNA that following fertilization of eggs that causes the delay in the process can be lethal to the embryo.
Paternal mitochondria in this type of roundworm have an internal self-destruct mechanism that gets activated when a sperm fuses with an egg. Delaying this mechanism, the scientists found, led to lower rates of embryo survival. By using electron microscope and tomography, the findings seen in the parental mitochondria that self-destruct that even before and they were engulfed by autophagosomes. When in RNA analysis the gene is removed the parental mitochondria persisted and resulting in increases the mortality. Dr. Xue and his colleagues found, however, that the paternal mitochondria in the roundworms actually started to break down before any autophagosomes reached them.
“It’s like a suicide mechanism,” said Byung-Ho Kang, a professor at the Chinese University of Hong Kong and another author of the paper. To test the importance of this gene, the team engineered C. eleganssperm 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.