Two mitochondria from mammalian lung tissue displaying their matrix and membranes as shown by electron microscopy. Photo: Louisa Thomas / Wikipedia
When it comes to mitochondrial inheritance, maternal genes rule the day at the expense of paternal ones. But why?
A new study, and led by 彩民宝典 researchers, sheds new light on a longstanding biological mystery.
Mitochondria are crucial to cellular processes, providing respiratory and metabolic functions that power a cell. Previous research has shown that nearly all animals inherit mitochondria exclusively from their mothers, while paternal mitochondria are selectively destroyed in fertilized egg cells. The exact mechanisms behind this process, however, have remained unclear.
After studying this phenomenon in nematodes (C. elegans), a multicellular roundworm commonly used for genomic studies, CU-Boulder researchers discovered that the worm鈥檚 male sperm commit a form of mitochondrial 鈥渟uicide鈥� shortly after fertilizing a female egg cell.
The male sperm mitochondria release an enzyme called endonuclease G that destroys its own mitochondrial DNA. The paternal mitochondria also lose their inner membrane integrity, which marks them for destruction by the egg鈥檚 own automatic disposal processes.
鈥淭he big surprise is that paternal mitochondria actively initiate their own demise very early in the process by releasing this endonuclease into the matrix to degrade the mitochondrial genome,鈥� said Ding Xue, a professor in CU-Boulder鈥檚 Department of Molecular, Cellular and Developmental Biology and senior author of the new study.
The findings mark the first time that researchers have observed and identified endonuclease G and its encoding gene (known as cps-6) as being responsible for paternal mitochondrial elimination in worms. The researchers indicate that human mitochondria have a similar endonuclease G, making it possible that the same process could be at work in humans.
The researchers also found that delayed removal of the paternal mitochondria in roundworms adversely affected the development of embryos, possibly due to incompatibility in cellular signaling.
鈥淭he results suggest that paternal mitochondrial persistence is evolutionarily disadvantageous,鈥� said Xue.
Co-authors of the new study include Qinghua Zhou, Haimin Li, Hanzeng Li, Akihisa Nakagawa, Eui-Seung Lee, Brian L. Harry and Riley Robert Skeen-Gaar of CU-Boulder; Jason L.J. Lin and Hanna S. Yuan of Academia Sinica (Taiwan); Shohei Mitani and Yuji Suehiro of the Japan Science and Technology Agency; Donna William of the University of Florida; and Byung-Ho Kang of the Chinese University of Hong Kong (China).
Funding for the study was provided by the National Institutes of Health, the March of Dimes and the Research Grants Council of Hong Kong.
Contact:
Ding Xue, 303-492-0271
ding.xue@colorado.edu
Paul Muhlrad, 303-492-0187
paul.muhlrad@colorado.edu
Trent Knoss, CU-Boulder media relations, 303-735-0528
trent.knoss@colorado.edu
