Although the gene has been identified in roundworms, and has yet to be confirmed in humans, the finding is thought to be significant because it marks the first time that the such a process has been observed.
Mitochondria are the energy centres of the cell and they contain a small amount of mitochondrial DNA (mtDNA). Unlike nuclear DNA, which is inherited from both parents, mitochondrial DNA is only inherited from the mother.
Prior to this study, it had been thought that maternal inheritance of mitochondria was driven solely by processes in egg cells that destroy paternal mtDNA.
Professor Ding Xue, from the University of Colorado-Boulder, a senior author on the study, which was published in the journal Science, said it was a 'big surprise [that] paternal mitochondria actively initiate their own demise' soon after fertilisation.
Professor Justin St. John, from the Hudson Institute of Medical Research in Australia, who was not involved in the study, told the New York Times that the research 'comes closest to elucidating a key development process that has perplexed us for a long time'.
The researchers studied the process of mitochondrial inheritance in the roundworm C. elegans using a combination of microscopy and genetic techniques. They found that an enzyme called endonuclease G degrades the inner wall of paternal mitochondria immediately following fertilisation and that this process started before egg-driven processes destroying the mitochondria got underway.
The scientists also carried out experiments where they cut the gene that encodes endonuclease G – called cps-6 – out of sperm, and used those sperm to fertilise C. elegans eggs. When they did this, the sperm mitochondria persisted longer in the early embryo and such embryos were less likely to survive.
Dr Vincent Galy, a researcher who uses C. elegans at Pierre and Marie Curie University in Paris, and who was not involved in the study, told the New York Times: 'This paper provides the first experimental data suggesting that it's not good to keep sperm mtDNA.'
The researchers report that human mitochondria have a similar endonuclease G, which makes it possible that the same process could be at work in humans. However, further research would be required to confirm that, they add.