Why our parasitic genes aren’t deadly

U. NOTTINGHAM (UK) — Researchers have discovered why so-called “jumping genes” found in most living organisms don’t ultimately kill their hosts.

The study reveals for the first time how the movement and duplication of segments of DNA known as transposons, is regulated. This prevents a genomic meltdown, and instead enables transposons to live in harmony with their hosts—including humans.

In the 1940s, Barbara McClintock discovered transposons, and received the Nobel Prize for Physiology or Medicine in 1983.

Ancient relics of these “jumping genes,” as they are sometimes called, make up 50 percent of the DNA in humans. They are characterized as “jumping” because they can change their position within the genome, thereby creating or reversing mutations.

This process, known as DNA transposition, plays a critical role in creating genetic diversity and enabling species to adapt and evolve.

Transposons don’t just jump from one location to another; they usually leave behind a copy of themselves at their original location. Left unchecked, this would lead to an exponential increase in their numbers. Exponential growth is always unsustainable, and in the case of transposons they would quickly kill their host.

Because this doesn’t happen, clearly some form of regulation is taking place within the genome. For a long time, scientists have understood that an enzyme called transposase, which is critical to the whole transposition process, also apparently brings it under control.

How this actually occurs has, however, remained a mystery — until now. For the first time, the new study, carried out by researchers at The University of Nottingham, The University of Cambridge and the Fred Hutchinson Cancer Centre in Seattle, successfully identified the mechanism through which DNA transposition is regulated.

Ronald Chalmers, professor of molecular and cellular biology at the University of Nottingham, says, “A successful parasite is not fatal to its host but lives in harmony with it. It was while doing some biochemistry research that we stumbled upon the solution. It was so simple that initially it was hard to appreciate the brilliance of it. It was a real forehead-slapping moment and seems a wonder that it was not discovered years ago.”

“In theory, transposons should just keep on increasing and kill us,” says Karen Lipkow, from the department of biochemistry at the University of Cambridge, and the Babraham Institute. “What we have identified is an ingenious mechanism which prevents this from happening by conferring autoregulation. The process is very simple, but it explains so much.”

A biochemical analysis of a mariner-family transposon from the human genome gave the first indication of the mechanism. As reported in the journal eLife, the team then expanded this concept using a computer model, which allowed them to simulate events on an evolutionary timescale, before carrying out further biochemical experiments.

Transposase is important to the genetic “jump” of transposons because it catalyzes the whole process. It does this by binding to specific sites at either end of the transposon, and then bringing these together to create a nucleoprotein complex that effectively performs a molecular cut and paste, moving the transposon DNA to a new location.

The study finds that once a certain number of copies of the transposon have been created, the transposase concentration rises above a critical threshold and begins to saturate its own binding sites. As clusters of the enzyme compete for binding, they interfere with each other and the transposition process is halted.

Using the computer model, the researchers were able to show that doubling the transposon copy number halves the rate of transposition. This is a crucial insight as it reveals an underlying self-righting mechanism for homeostasis. In a nutshell, it makes the transposon’s genetic burden on the host constant and predictable, and brings an uneasy harmony to the relationship.

Source: University of Nottingham

chat6 Comments


  1. Roy Niles

    This is one of those neoDarwinistic explanations where the argument would also seem or need to be that functional systems in life are accidentally constructed by nature to appear to be intelligently done.

  2. Shawn

    No it’s not a neoDarwinistic explanation. It’s the discovery that these genomes have a unknown yet to be discovered variable that stops them from replicating more of that DNA material killing the host. Just because the reason for this has not yet been discovered does by no means imply that it was a higher power. We have the power to make life, alter it, destroy it and help it and nearly any ability “claimed” that “God” could do as well. I’m always open to new ideas as long as trial, verifiable facts and tests can prove or disprove the “claim.” Science is by no means always right, but they test and try the theories to find out the “truth” or facts about things. Without failing we can never learn.

  3. Roy Niles

    Who said anything about a higher power? If your argument is that biological systems weren’t constructed by the organisms initially, what is it you propose that did it? And if their systems were, as seems obvious, constructed over time by the organisms, how was that work done at all intelligently unless it was through the intelligence of those very organisms who evolved the capacity to use their strategies constructively?
    Obviously you don’t like the implication that you’re arguing on behalf of the accidental development of intelligent systems, but what’s your alternative except to recognize that biological systems have supplied their own intelligence from the start?

  4. Mike

    Well, Roy, genetic success is not “accidental,” unless the survival of systems or organisms that are better adapted for environments where others have failed and fallen away is an accident; it’s simply a favorable evolutionary outcome, where others have not been. Successful systems or organisms “appear to be intelligently done” because they’re the ones that are left to study. The ones that WOULDN’T appear to be intelligently done are no longer around. Biological mechanisms that succeed aren’t “intelligent,” they’re just viable and well-adapted. Successful vs unsuccessful outcomes based on random generational mutation in species populations are well-observed, and settled science. Get used to it, or offer a solidly crafted and convincingly tested Intelligent Design alternative to “neoDarwinism.” What? There’s no such thing, and hasn’t ever been, despite decades of time and opportunity to develop one? I guess we can see which system has the problem, then, can’t we?

  5. Roy Niles

    “Successful vs unsuccessful outcomes based on random generational mutation in species populations are well-observed, and settled science.”
    Was that supposed to be an explanation as to how the organism’s physical systems were constructed without the organism itself doing any of the work? How do random mutations construct anything? My understanding was that they cause changes, but no one of your tribe has yet explained how those changes have been constructive in a way that replaces or at least repairs what the mutations have accidentally changed.
    If you want an alternative to a belief in stochastic slight of hand, you should at least have the curiosity to look for one. And if you looked, you would find that the theories of adaptive mutation and self-engineering are blooming.

  6. Villainess

    You need to re-read the article. The process IS now understood, and I thought fairly clearly explained.

    1) there’s not an infinite number of sites the transposons can jump to.
    2) when they reach a certain saturation level, they start to interfere with eachother, slowing down
    3) this interference ultimately creates a cap on the total number of copies that can be made in any DNA set

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