The sex of human and all mammalian babies may be determined by a simple modification of a virus that insinuated itself into the mammalian genome as recently as 1.5 million years ago, a new Yale University-led study has found. 
 
 “Basically, these viruses appear to allow the mammalian genome to continuously evolve, but they can also bring instability,” said Andrew Xiao of the Department of Genetics and Yale Stem Cell Center, senior author of the paper published online March 30 in the journal Nature. “Aside from the embryo, the only other places people have found this virus active is in tumors and neurons.” 
 
 Xiao and the Yale team discovered a novel mechanism by which the early embryo turns off this virus on the X chromosome, which ultimately determines the sex of an organism. If the level of this molecular marker is normal, X chromosomes remain active, and females and males will be born at an equal ratio. If this marker is overrepresented, X chromosomes will be silenced, and males will be born twice as often as females. 
 
 “Why mammalian sex ratios are determined by a remnant of ancient virus is a fascinating question,” Xiao said. 
 
 Tens of millions of years ago viruses invaded genomes and duplicated themselves within the DNA of their hosts. Xiao estimated that more than 40% of the human genome is made up of such remnants of viral duplications. In most cases, these remnants remain inactive, but recently scientists have discovered they sometimes take on surprising roles in developing embryos and may even push mammalian evolution. Researchers found that the virus active in the mouse genome that influences sex ratios is relatively recent — in evolutionary terms — and is enriched on the X chromosome. 
 
 The Yale-led team found the mechanism that disables the virus. The newly discovered modification in mammals is a surprising expansion of the epigenetic toolbox, say the researchers. Epigenetics modulates gene expression during development without actually altering the sequences of genes. In the new marker, a methyl bond is added to adenine — one of the four nucleotides that comprise base pairs in DNA — allowing it to silence genes. For decades, most researchers assumed that a modification of the nucleotide cytosine was the only form of gene silencing in mammals. 
 
 Xiao said it is possible that this mechanism might be used to suppress cancer, which has been known to hijack the same virus to spread. 
 
 He also noted in other organisms, such as C elegans and the fruit fly Drosophila, this mechanism plays an entirely opposite role and activates genes, not suppresses them. 
 
 “Evolution often uses the same piece but for different purposes and that appears to be the case here,” Xiao said. 
 
 Tao P. Wu of Yale is the lead author of the study. 
 
 Pacific Biosciences of Menlo Park provided the technology used in the discovery. 
 
 Primary funding for the research was provided by the National Institutes of Health. ||||| It's a boy! Or maybe it's a girl, but either way, new research suggests that the sex of mouse babies, and perhaps the sex of human babies, may be influenced by a newfound way to deactivate ancient viral genes that have been embedded in mammal genomes for more than a million years. 
 
 In the research, the scientists looked at viral DNA that is active in the mouse genome. Viral DNA can become part of an animal's genome when a kind of virus called a retrovirus infects a cell, and slips its genes into the DNA of host cells. (The most notorious retrovirus is HIV, the virus behind AIDS.) 
 
 If a retrovirus infects a sperm or egg cell — and that sperm or egg is involved in fertilization and becomes part of a person — all of the person's cells will have the viral DNA, and they will pass it on to their descendants. Hence, people and animals today carry in their cells the genetic remnants of viruses that invaded the genomes of their ancestors. 
 
 In fact, more than 40 percent of the human genome may be composed of viral "leftovers," said Andrew Xiao, the senior author of the new study and a molecular biologist at the Yale School of Medicine in New Haven, Connecticut. 
 
 Most viral remnants are inactive. But some viral DNA "can interfere with development or health," Xiao told Live Science. And it could also accelerate mammalian evolution, he said. For example, if an organism faces changes in the climate or its food source, viral DNA may introduce variations that help the organism adapt to the change. 
 
 In the new study, the scientists found high levels of a viral remnant on the mouse X chromosome, which helps determine the sex of mice. If this viral DNA is active, X chromosomes stay active, and females and males are born at an equal ratio. However, if this viral material is silenced, X chromosomes will get deactivated, and males will be born twice as often as females, according to the findings, published in the March 31 issue of the journal Nature. 
 
 Although it remains uncertain whether a similar mechanism influences human sex ratios, the human X chromosome also contains viral material, Xiao said. [The 9 Deadliest Viruses on Earth] 
 
 The researchers also discovered how the mouse cells deactivate the viral genetic material in order to shut down the X chromosome. Cells commonly deactivate genetic material by attaching a compound known as a methyl group to the DNA. This methyl "tag" influences genetic activity without changing the genetic sequence itself. The gene is shut down, while the sequence of A, T, G and C nucleotides remains intact. 
 
 But Xiao and his colleagues found that mouse embryo cells add a methyl tag to the nucleotide A, or adenine, to silence the viral genes. For decades, scientists thought the only way to silence a gene in mammals was to tag a C nucleotide, or cytosine. 
 
 Although scientists knew for a long time that single-celled organisms could tag the A nucleotide, "this is the first time it's been seen in mammals," said Gerd Pfeifer, a molecular biologist at the Van Andel Research Institute in Grand Rapids, Michigan, who did not take part in this research. 
 
 Aside from helping determine the sex of offspring, the viral material the researchers studied has been shown to potentially help tumor cells grow, and to be active in the brain, Xiao said. [7 Diseases You Can Learn About from a Genetic Test] 
 
 The researchers are still investigating which enzyme tags the A nucleotides. "We also want to find out how this mechanism might be involved in human health," Xiao said. 
 
 This new work revealed that this tagging of adenine is very rare in the mouse genome, only affecting "about seven out of every million adenines," Pfeifer said. Future research should further investigate whether this tagging is more common in some tissues than in others, Pfeifer added. 
 
 Follow Charles Q. Choi on Twitter @cqchoi. Follow Live Science @livescience, Facebook & Google+. Originally published on Live Science. ||||| NEW HAVEN, Conn., March 31 (UPI) -- Over the course of human evolution, the human genome has picked up foreign fragments of DNA, mostly from ancient viruses. 
 
 The majority of those fragments are inactive, but a few serve novel purposes -- like determining the sex of a developing embryo. 
 
 Yale researchers believe an ancient viral DNA strand -- incorporated into the mammalian genome as recently as 1.5 million years ago -- plays a key role in turning off the X chromosome. 
 
 Scientists at Yale University determined that some embryos turn off the virus on the X chromosome, affecting sex ratios, and discovered the mechanism by which they do it. In the epigenetic marker they found, a methyl bond is added to adenine, one of the four nucleotides that form DNA base pairs, producing a gene-silencing ability. 
 
 Higher levels of the marker turn off the virus, silencing X chromosome expression, and males are born at a ratio of 2-to-1. When the molecular marker is normal, males and females are born in equal numbers 
 
 "Why mammalian sex ratios are determined by a remnant of ancient virus is a fascinating question," Andrew Xiao, a geneticist at the Yale Stem Cell Center, said in a news release. 
 
 Xiao is the senior author of a new paper on the discovery, published this week in the journal Nature. 
 
 Until recently, researchers believed mammals could suppress gene expression via manipulation of nucleotide cytosine. 
 
 Xiao and his colleagues think the newly discovered mechanism may be used to suppress cancer, as previous studies suggest cancer can hijack the virus in an attempt to spread. 
 
 "Aside from the embryo, the only other places people have found this virus active is in tumors and neurons," Xiao said.
– The sex of baby mice—and quite likely baby humans—is determined by a virus that inserted itself into the mammalian genome 1.5 million years ago, Live Science reports. Yale researchers published their surprising findings on March 30 in Nature. According to a press release, more than 40% of the human genome is comprised of remnants from viruses that invaded it millions of years ago. Researchers found some of that viral material on mice X chromosomes—the chromosomes that determine the sex of embryos. As long as that viral remnant is active, males and females are born at equal rates. But if the viral remnant is turned off, which UPI reports happens in some embryos, males are born at twice the rate of females. While it's unclear if the same process holds for humans, the human X chromosome contains the same viral material as its mouse counterpart. What's more, researchers believe the method by which mice embryos turn off the viral remnant could be used to keep cancer from spreading. That's because the same viral material is also found in tumors and could be helping them grow. But really they're still trying to figure this whole thing out. "Why mammalian sex ratios are determined by a remnant of ancient virus is a fascinating question," says esearcher Andrew Xiao. (Thanks to genetics, girls in this town become boys at puberty.)