Is Junk DNA Really Junky? A Fish-Eating Plant Weighs In.

What Have We Learned?
Oct. 3 2013 8:31 AM

Is Junk DNA Really Junky?

The delicious, religious debate over what most of our genome is good for.

The silk dancers' interpretation of DNA loops.
Dancers' interpretation of DNA loops

Courtesy of Tom Whipps/Nature

In the 12 years since the human genome was sequenced, so many critters have had their DNA deciphered—oysters, bees, eels, camels, clawed frogs, elephant sharks—that it’s hard to suppress a yawn sometimes. But every so often, a genome cuts through the indifference and makes geneticists’ eyes goggle out. Take the humped bladderwort, a humble aquatic plant whose DNA was sequenced this past May.

The humped bladderwort has yellow, snapdragon-like flowers, and it’s actually carnivorous, capable of trapping and eating not just insects but even tadpoles and tiny fish. But this combination of beauty and death isn’t what makes the bladderwort special. Most organisms have loads of junk DNA—less pejoratively, noncoding DNA—cluttering their cells. The bladderwort doesn’t: 97 percent of its DNA is classic, hardworking, protein-building DNA. And that lean, mean bladderwort DNA challenges some trendy notions about how all DNA works, including (if not especially) in human beings.

First, a primer on junk DNA, one of the most reviled terms in science. Anyone who took Bio 101 remembers (if only vaguely) that DNA gets turned into RNA, which in turn gets turned into proteins. The protein-producing stretches of DNA are called genes, and genes reside on much longer molecules called chromosomes.

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A century ago, as biologists came to grips with the vast number of different proteins needed to build and maintain the body, they decided that genes must be packed very tightly together on chromosomes, since tight packing would be more efficient. They couldn’t have been more wrong. In humans, a typical species in this regard, less than 2 percent of our 3 billion letters of DNA actually builds proteins. Chromosomes were more like vast Saharan wastelands, broken up only sporadically by oases of genes.

So what does that extra 98 percent do? Here’s where things get contentious. Some of the excess—the pseudogenes, the transposons, the tedious stretches where Mother Nature held her fingers down on the keyboard (ACACACACACA ... )—does look like garbage. Heck, 8 percent of our genome is nothing but old, broken-down virus DNA, the genetic equivalent of a Pontiac Firebird on cinderblocks. The name junk DNA emerged in the early 1970s as a catchall term for this cruft.

Even at the time, though, some scientists objected to the term as too dismissive. Molecular biologists had already discovered bits of junk that, far from being irrelevant, actually managed genes: They turned genes on or off and regulated when and where genes were active. As more and more examples of this type of control emerged in the 1980s, the term junk DNA seemed less and less appropriate.

The protests grew especially loud after the Human Genome Project decided (somewhat arbitrarily) to declare the genome fully sequenced in 2003. Before, most geneticists argued that, based on our size and smarts, human beings must have around 100,000 genes. The Human Genome Project turned up just 23,000. (That’s fewer than the bladderwort’s 28,500, incidentally.) Biologists now faced a doozy of a dilemma: How can a species as complex as Homo sapiens get by with so few genes?

One good bet was noncoding DNA. Again, noncoding DNA can switch genes on or off or make them produce proteins faster or slower. It also helps splice and remix genetic material, allowing different types of cells (neurons especially) to customize their RNA and proteins. In other words, noncoding DNA allows us to use one gene in many ways, multiplying the effective number. Perhaps, then, it wasn’t genes alone that made human beings special; it was how we used genes that counted.

Noncoding DNA also offered new leads on curing diseases. Frankly, the sequencing of the human genome hasn’t lived up to its hype here: Almost no new treatments have emerged, and there aren’t many in the pipeline, either. Things look especially bleak for common killers such as diabetes and heart disease. Those ailments clearly have a genetic component. But when scientists survey genes looking for which mutations patients have in common, they come up empty. In other words, far from curing these diseases using genetics, scientists can’t even find the right DNA to target. Geneticists are still hashing out the details of why this approach whiffed, but part of the problem could be a failure to understand how noncoding DNA contributes to diseases.

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