made its discovery while studying piggyBac, an active cut-and-paste jumping gene from insects. PiggyBac got its name because it hitched a ride from one host to another on a virus. While studying how the jumping gene works, the researchers also used computational methods to search for piggyBac-like DNA sequences in the genomes of some species, including that of the little brown bat. There they found a sequence similar to piggyBac, one that didn't appear to have collected mutations that would make it inactive. Sure enough, near-identical copies were sprinkled throughout the genome, indicating that the sequence had jumped relatively recently. Craig named the find piggyBat. Her team also found that piggyBat can move within bat cells, other mammalian cells and yeast, showing that it is indeed a still-active DNA element.
Many organisms have developed systems to decrease the frequency at which jumping genes move, Craig says. Such systems are a component of immunity, protecting mammals from retroviruses, as well as from the risk that jumping genes will wreak havoc by interrupting an important gene.
Over time, the protective systems have made most mammalian jumping genes inactive. The finding that a bat species is host to an exception, combined with the fact that bats are particularly susceptible to viruses, may indicate that the systems that protect us from dangerous genetic material are not as well-developed in bats, Craig says. But whatever the reason for its presence, piggyBat "opens up a window for studying jumping gene regulation in a mammal where the element is still active," she says.
This future research should yield insights on the workings of jumping genes themselves, as well as on the protective systems that keep them in check, Craig says. Ultimately, her group hopes to custom-design jumping genes that can be used for targeted, safe and effective gene therapy, delivering genes needed to treat disease.
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