The Jumping Gene: Friend or Foe?

A cob of maize holds several hundred kernels, and each one came from its very own fertilization. So you could think of the cob, perhaps, like a large, tight-knit family, full of unique kernel personalities: some purple, some yellow, some fat, some skinny.In the 1940s, geneticist Barbara McClintock of the Cold Spring Harbor Laboratory in New York wanted to know: Why is it that some kernels show an uneven splattering of color? If the DNA in every cell in each kernel contains the same pigment gene (or genes), then why isn’t that color expressed the same way in every cell?As McClintock would discover (and, three decades later, win a Nobel Prize for), the color variation in maize comes from transposons, or so-called jumping genes. These stretches of DNA hop out of their original spot in the genome and then wedge themselves in another, random place. When they land, they may disrupt the activities of nearby genes, including pigment genes. The jumping patterns are different in every cell, thus explaining the color variability.Ever since McClintock’s big discovery, two ideas have dominated the scientific literature on jumping genes, notes Josh Dubnau, a neuroscientist at Cold Spring Harbor. One is that transposons are, in a sense, friendly. For example, as I wrote about a couple of weeks ago, a recent study found that jumping genes are more active in some types of neurons than others, suggesting that the brain has evolved ways of using these elements for its own (normal, healthy) specialization.The other idea is that, while transposons may be useful in certain circumstances, they’re usually parasites. Studies have shown that when transposons jump in stem cells that become sperm or egg cells, for example, “they can destroy the germline. You can get animals that are completely sterile simply because a transposon has gone rogue,” Dubnau says. “This is the dark side of transposons.”Read more at...Only Human, April 2013.