(CN) — No one ever wants to come down with a virus. But in the long haul, new research suggests, viruses play a major role in differentiating and fine-tuning mammals’ genomes — even to the benefit of species’ reproductive capacities.
“What we learn from our study is that, in general, viruses have major roles in driving evolution,” Satoshi Namekawa, the principal investigator behind two papers published Monday in Nature Structural & Molecular Biology, said in a statement. “In the long-term, viruses have positive impacts to our genome and shape evolution.”
Namekawa, a scientist at Cincinnati Children’s Hospital Medical Center’s Division of Reproductive Science, examined lab mice and human germline cells to explore viruses’ role in shaping mammals’ survival.
An organism’s germline is its sex cells, male or female, whose genetic information is mingled with other sex cells’ information and passed down to its offspring as inherited genetic material. A germline’s transcriptome is the set of all the messenger RNA in the germline’s cells – in other words, all that an organism has to offer for the next generation as inheritable genetic material.
“A transcriptome is basically encoding the functions of all the cells,” Namekawa said in an interview with Courthouse News. “Each transcriptome needs to be very unique in the cells, and also the germline transcriptome needs to be very specialized in each species, because each species should have unique reproduction.”
Mammals’ transcriptomes, the two studies show, were fine-tuned over generations by a certain kind of virus: endogenous retroviruses, or ERVs, relics of ancient viral infections that weaved their genetic sequences into mammals’ genomes over millions of years.
“[A virus] can be basically integrated into the DNA of our genomes. Once integrated, it can ‘jump around’ our genomes,” Namekawa said. “This way, they can modify the host’s genome by jumping around.”
These ERVs are called “jumping genes” because they can change places with other portions of a genome. Between 40 and 50% of any given mammal’s genome is composed of these jumping genes, which contributed to species differentiation at the molecular level.
“Gene regulation in the germline ensures the production of high-quality gametes, long-term maintenance of the species and speciation,” the authors wrote in their study on ERVs.
Namekawa and his colleagues found that after male mice’s sex cells undergo meiosis, certain ERVs enhance and regulate spermatogenesis — the development of sperm cells — and suggest that similar processes occur in humans as well.
“Of note, independently evolved ERVs are associated with the expression of human-specific germline genes, demonstrating the prevalence of ERV-driven mechanisms in mammals,” the authors wrote. “Together, we propose that ERVs fine-tune species-specific transcriptomes in the mammalian germline.”
Namekawa worked with his colleagues at the Cincinnati Children’s Hospital as well as researchers from Tokyo University and Azabu University in Japan and the University of Vienna — in all, more than a dozen bioinformaticians, developmental biologists and immuno-biologists ranked among the authors.
The other study concerned super-enhancers, which are essentially robust regulatory elements in the genome. They power bursts of germline genes when sperm begin to form in males.
“We basically profiled the locations of active enhancers for the genome at different stages of spermatogenesis,” Namekawa said. “This study is showing the gene expression mechanism in male germ cells.”
The investigators analyzed mice’s male germline — the cells of their testes, which express thousands of germline-specific genes — and found that super-enhancers’ genome-wide reorganization drive bursts of gene expression during meiosis, the sexual reproduction process where one sex cell divides into four sperm or egg cells, each with one copy of each chromosome.
The scientists identified two molecular events that occur during these genetic processes, finding what factors enhance cell division in mammals’ germlines and ultimately contribute to the diversity and complexity of the testes’ transcriptome.
Species with diverse and complex genomes benefit from genetic resilience as a result, but that isn’t the end of the story for the researchers’ findings. They represent a look into how strange and surprising the mechanisms of species differentiation and evolution are.
“Especially this endogenous retrovirus study … will facilitate our understanding of evolutionary biology, because this is a key mechanism to defining the identity of species,” Namekawa said.