Evolving from free-swimming bacteria engulfed by forms of humans’ earliest ancestors billions of years ago, almost every human cell is powered by mitochondria, which use oxygen to create usable energy for our body’s daily needs. Originating from free-floating bacteria, mitochondria have unique DNA different from the 23 pairs of chromosomes in our body. Although our chromosomes come from both parents, 23 each, nearly all humans’ mitochondrial DNA (mtDNA) comes from the mother’s egg. What about the mtDNA in the sperm cell then? DNA rendering

Scientists figure that sperm’s mitochondria are soon broken down by molecular processes after fertilization in other animals, but the reason behind why this happens to humans has been unknown. Now research has found that human sperm’s few mitochondria contain virtually no DNA at all. This mtDNA elimination process might play a role in human infertility and mitochondrial diseases, according to molecular biologist Dmitry Temiakov of Thomas Jefferson University in Philadelphia. Coming up with the same conclusion, Shoukhrat Mitalipov, Ph.D., director of the Center for Embryonic Cell and Gene Therapy at OHSU, said, “We found that each sperm cell does bring 100 or so mitochondria as organelles when it fertilizes an egg, but there is no mtDNA in them.” Using molecular biology, researchers found that sperm’s mitochondria did contain some DNA, along with an important protein called mitochondrial transcription factor A (TFAM) that acts to protect that DNA. But after the sperm cells mature, chemical changes happen which prevent TFAM from entering mitochondria, and as it enters the nucleus instead, it no longer prevents the mtDNA from degrading. The fact that DNA damage in sperm from oxidative stress is common could be another reason why mitochondrial DNA disintegrates. Having mitochondrial DNA doesn’t help fertility either; if the sperm’s mitochondrial DNA sticks, it could become a source of infertility. Previous studies showed that sperm cells with elevated amounts of mtDNA experience decreased sperm counts and motility. A new study found that other animals “show multiple mechanisms that may contribute to maternal mitochondrial inheritance in different organisms,” said Xinnan Wang, a mitochondrial cell biologist at the Stanford University School of Medicine. This study connects to our lesson in AP Biology on the concept of genetics and how our DNA is passed on from our parents. Specifically, we previously learned how our mitochondrial DNA is almost completely from our mother, as the egg contains way more mitochondrial DNA than the sperm, allowing us to track ancestry by maternal mitochondrial DNA. This study expands our understanding of this concept. According to Temiakov, there are probably other unidentified mechanisms in sperm cells that regulate mtDNA, as a future area for research as it is crucial to better understand mitochondrial diseases and how to treat them. What do you think would happen if the mtDNA is passed on equally from both parents?​​​

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