What’s the News: We’ve long had signs that when it comes to inheritance, DNA isn’t the be-all, end-all. Trees that have the exact same genes but were raised in different greenhouses behave differently. Worms with genes that impart long life can pass on that longevity to their progeny—even if they don’t pass on the genes. Both of these phenomena, we’ve discovered, come from epigenetic changes in tags attached to DNA that control whether genes get expressed.
But every now and then we get a whiff of other possible routes for inheritance, even stranger than that. A new paper in Cell reports that worms whose grandparents had the ability to fight viruses using a fleet of tiny RNA molecules retain these molecules even when they don’t have the genes for them. They can pass these molecules down for more than a hundred generations.
RNAs from rice can survive digestion and make their way into mammalian tissues, where they change the expression of genes.
What’s the News: It’s no secret that having lunch messes with your biochemistry. Once that sandwich hits your stomach, genes related to digestion have been activated and are causing the production of the many molecules that help break food down. But a new study suggests that the connection between your food’s biochemistry and your own may be more intimate than we thought. Tiny RNAs usually found in plants have been discovered circulating in blood, and animal studies indicate that they are directly manipulating the expression of genes.
Early Earth’s chemical seas are presumed to have given rise to the first life, but how could anything so complex have come from such a disorganized stew of molecules? That’s the question Gerald Joyce of the Scripps Research Institute is exploring with his swarms of self-replicating RNA, which can evolve over time. Along with Steve Benner, Craig Venter, Jack Szostak, and others, he is on the road to creating life in the lab, thus giving us insight into both our origins and what, exactly, “life” is. As Dennis Overbye writes in a look at the field in the New York Times:
The possibilities of a second example of life are as deep as the imagination. It could be based on DNA that uses a different genetic code, with perhaps more or fewer than four letters; it could be based on some complex molecule other than DNA, or more than the 20 amino acids from which our own proteins are made, or even some kind of chemistry based on something other than carbon and the other elements that we take for granted, like phosphorous or iron. Others wonder whether chemistry is necessary at all. Could life manifest itself, for example, in the pattern of electrically charged dust grains in a giant interstellar cloud, as the British astronomer and author Fred Hoyle imagined in his novel “The Black Cloud”?
The problem: Scientists want to study our circadian rhythms, our bodies’ internal clocks, and they can do so on the genetic level by examining how gene expression changes throughout the day. But ordinarily that would require sampling a person’s blood or skin multiple times a day, an ordeal few of us would want to endure.
The solution: hair.
Makoto Akashi’s team reports today in the Proceedings of the National Academy of Sciences that hairs, be they from the beard or head, contain the telltale signature of RNA activity that shows when we humans are at our peak activity level for the day.
In a medical sense, you’d be wise to steer clear of filoviruses, a group that includes the deadly Ebola, and bornaviruses, which cause neurological diseases. But in a genetic sense, it may not be possible to avoid them. A new study in PLoS pathogens shows that bits and pieces of these viruses have been floating around in the human genome, as well as those of other mammals and vertebrates, for millions of years.
It’s not that having genetic material left behind by viruses is odd—previous research had shown that viruses account for 8 percent of the human genome. But scientists thought most of that material came from retroviruses, which use their host’s DNA to replicate and leave some of their genetic material behind. What’s weird about this is that filoviruses and bornaviruses are not retroviruses—they’re RNA viruses, which don’t use the host to reproduce in the same way.
It’s still out there, you know.
A study out today in the journal Science tracks the path of swine flu, which may have receded from the forefront of humanity’s attention but hasn’t quit mixing and moving and making ready. The scientists led by virologist Malik Peiris say the flu virus that the world feared last year has gone back into pigs in China, where it’s laying down and recombining its genetics with other flu strains. And, they say, we’re not sufficiently monitoring the danger of a new strain jumping back to people.
“Just because we’ve just had a pandemic does not mean we’ve decreased our chances of having another,” said Dr. Carolyn B. Bridges, an epidemiologist in the flu division of the Centers for Disease Control and Prevention. “We have to stay vigilant” [The New York Times].
So far in 2010 we’ve seen nanotubes that carry thermopower waves to create electricity, nanoparticles that latch onto only damaged cells to deliver drugs there, and more. Today there are a couple more clever uses for nanotechnology—taking the salt out of salt water, and nanobots that deliver gene therapy.
In Nature Nanotechnology, an MIT team showed they could use nanotech to desalinate water in a new way. At the moment, desalination plants employ reverse osmosis, in which pressure forces the salt ions through a membrane. But this process is an energy-gobbler and the membrane is prone to clogging, which means that de-sal plants are inevitably big, expensive, fixed pieces of kit [Sydney Morning Herald].
Odds are, you have it. By the age of 40, nearly 90 percent of adults in the United States have been exposed to the herpes simplex virus-1 (HSV1) that causes cold sores. Not everyone who has the virus lurking in their body will have symptoms, but those who do will be annoyed for life by unexpected lip blisters. But now the secret of how the cold sore virus manages to persist for a lifetime in the human body may have been cracked [BBC News], and researchers say their findings may point the way towards a treatment that could kill the virus once and for all.
The virus is a difficult target. When a cold sore appears, it’s easily treatable with a drug that kills the replicating virus, but that drug can’t get to the latent versions of the virus that are hiding within nerve cells and waiting to cause the next eruption. Until now, research has generally concentrated on keeping HSV1 inactive — and preventing cold sores from ever showing up. But [Duke University] researchers took the opposite tack: figuring out precisely how to switch the virus from latency to its active stage. That’s important, says lead author Dr. Bryan Cullen, professor of molecular genetics and microbiology at Duke, “because unless you activate the virus, you can’t kill it” [Time].