Why transposons are not actually jumping genes

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An interdisciplinary institute dedicated to transformative research and technology in life sciences using team-based strategies to tackle grand societal challenges. This result emerged from studies conducted at the University of Illinois at Urbana—Champaign, where scientists were dissatisfied with existing methods for studying jumping genes, or transposable elements TEs.

Rather than rely on these methods, which are bulk techniques that average results from multiple cells, the scientists developed a fluorescent protein—based reporting system that allowed them to focus on individual cells. That way, instead of having to make do with time and cell ensemble averages, the researchers could capture cell-to-cell variation and temporal variability in individual cells.

In short, the scientists found a way to observe jumping genes in action directly, in real time. Upon entering stationary phase, TE activity increases in cells hereditarily predisposed to TE activity.

To observe individual TE events in living cells, the scientists devised a synthetic biological system based on the bacterium Escherichia coli. The scientists coupled the expression of fluorescent reporters—genes that encode in this case, blue and yellow fluorescent proteins—to the jumping activity of the transposons.

The scientists could then visually record the transposon activity using fluorescent microscopy. Some tumors also had none; there's a lot of variation. Transposons fall under two broad categories: DNA transposons and retrotransposons. Retrotransposons leave the original transposon intact and move by copying and pasting, rather than the cutting and pasting process of DNA transposons.

There is no limit to the number of retrotransposons, due to the fact that they copy themselves each time they move. With retrotransposons, the transposon is transcribed to make an RNA intermediate, which is then reverse transcribed into DNA, then inserted into the chromosome in the genome.

Different organisms have different active transposons. Humans have only a few kinds of retrotransposons. Mice, however, have several active families of retrotransposons, and fruit flies have dozens. The study of transposons has increased as new techniques have made it easier to find them. In recent years, researchers at Johns Hopkins studied transposons in tumors, mapped them in the genomes of many people and studied them in other animals. One could imagine a transposon inserting itself into a beneficial gene—a tumor suppressor, say—and silencing it.

Transposons have other ways of disrupting the genome. They can promote recombination, meaning they provide sites with matching DNA on different chromosomes that make it easier for the chromosomes to swap DNA. That can put whole segments of chromosomes where they don't belong. It seems logical that transposition could contribute to cancer. They may just be followers," Kazazian says. Other researchers have found active LINE-1s in lung cancer. 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.

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. 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.

Dubnau has provided another example of transposon terror in a study published earlier this month in Nature Neuroscience.

His team found that in normal fruit fly brains, jumping genes accumulate and become more active with age. His study focused instead on a type of jumping gene that is active in people. Take, for example, our argonaute family of proteins, which can latch on to jumping genes and shut them down.