The day, some 4.5 billion years ago, was just five hours long, but it was a momentous one for Earth. A Mars-size object roaring in at 40,000 km/h struck the young planet, already largely formed but devoid of life. The glancing blow hurled molten and vaporized debris into space, where it cooled, began circling Earth and eventually coalesced to form the moon.
This scenario, reported in the journal Nature last month, is drawn from a new computer simulation that goes far toward resolving puzzling inconsistencies in earlier studies of the moon's formation. That event was, of course, of overwhelming importance in our planet's history, since it reduced Earth's rotational wobble and set the stage for ocean tides and ultimately life, not to mention untold moon-June poesy. Earlier simulations required a much larger object crashing into an Earth only partly formed and spinning too fast to explain Earth's current rotational rate-our 24-hour day. One study needed two separate impacts to scale back the spin rate.
To get at these ancient events, Robin Canup of the Southwest Research Institute in Boulder, Colorado, and Erik Asphaug of the University of California at Santa Cruz re-enacted them in their computers by taking into account such factors as gravity, impact shock, melting and vaporization. They also created models with a finer level of detail than earlier efforts. Finally, after a number of tries, they arrived at a scenario in which an object, the size of Mars but with only one-tenth the Earth's mass, striking at a highly oblique angle, ejected enough debris from itself and our planet's iron-deficient outer layers to form the moon, which contains very little iron. Left behind was an Earth roughly the size it is today.
Apart from satisfying our curiosity about how the moon formed, the new work has broader implications. Explains Asphaug: "It's now known that giant collisions are a common aspect of planet formation, and these big impacts might go a long way toward explaining the puzzling diversity observed among planets." That diversity was recently emphasized when astronomers using the University of California's Lick telescope reported the discovery of two planets in orbit around a distant star. Unlike all previously discovered extra-solar planets, which have highly elliptical orbits, these two were moving in nearly circular paths. Alas, even the best telescopes are not sensitive enough to detect any extra-solar moons.
Most of the scientists who gathered in Washington last month to talk about human cloning agreed that cloning an entire human being-besides being morally questionable-was fraught with technical obstacles. After all, research into animal cloning has already shown that for every apparent success like Dolly the sheep, there are hundreds of failures, including many badly deformed creatures that were usually miscarried.
Now comes word that it might be easier to clone humans than was previously believed. According to research at Duke University, people have a genetic quirk that might prevent some of the developmental deformities associated with animal cloning. "That doesn't mean there aren't other things that could go wrong," says Randy Jirtle, a professor of radiation oncology at Duke
and one of the study's authors (who hastens to add that he has no intention to try such cloning). "But humans may be less susceptible to these kinds of [mishaps]."
To understand why, you need to know about a curious feature of some genes. Except for the genes that occur on the sex-determining X and Y chromosomes, it generally doesn't matter whether you inherit a particular stretch of DNA from your mother or your father. In the past 15 years, though, researchers have learned that at least 50 pairs of these so-called autosomal genes act a little differently. In a process called imprinting, one of each pair is permanently turned on or off, depending on whether it derives from the sperm or the egg.
As a rule, genes imprinted by the father would, if they worked in isolation, favor larger fetuses-presumably to give them a better shot at survival. The mother imprints the genes in such as way as to favor smaller fetuses-presumably so she'll have enough strength to bear more than one child. Usually a stalemate ensues between the competing imprinted genes because one gene is turned on and one turned off, and the babies are born just the right size.
During cloning, however, most of these imprints are wiped out and have to be reset-that is, turned on or off. Chances are that some won't be reset properly, which could lead to severe birth defects.
What the Duke researchers showed is that one gene, called IGF2R, which helps brake growth, is normally imprinted in sheep, cows and mice but not in humans. Human clones would always inherit nonimprinted IGF2R genes, so there would be no chance of a mix-up and, at least in this respect, their growth would be normal. But what of the other 49 or so imprinted genes? No one knows what trouble they might cause. So the fact that humans have one less imprinted gene than mice, sheep or cows means that human cloning might be marginally easier, but not necessarily safer.