Can jumping genes explain biological complexity?
Research finds genes that boost complex cells are lethal to simpler ones. Stephen Fleischfresser reports.
A previously overlooked relationship between jumping genes and DNA repair mechanisms might be behind the evolution of biological complexity that saw the emergence of life as we know it, argues new research published in the journal Proceedings of the National Academy of Sciences.
Barbara McClintock first discovered that elements of DNA can move around the genome, a finding that won her a Nobel prize in 1983.
These are known as transposable elements or “transposons”. The most numerous class of them, making up about half of the human genome in the form of so-called junk DNA, are called “retrotransposons”, or jumping genes. These are sequences of DNA that can copy and paste themselves throughout a genome, multiplying as they do so.
Retrotransposons are common in the most recent of the three domains of life, the eukaryotes, to which all plants, animals and fungi belong. They are far rarer in the other two domains, bacteria and archaea, and this is something of a curiosity because jumping genes evolved from mobile genetic elements known as “group II introns” – which are endemic to bacteria.
A related curiosity is that the number of genes an organism has doesn’t equate to biological complexity. The commonly used research model organism, Caenorhabditis elegans, a tiny roundworm, has the same number of genes we do, for example.
This has led to the hypothesis that the invasion of genomes by transposable elements before the last eukaryotic common ancestor was one of the early evolutionary events that shaped the domain.
This increase in biological complexity is thought to hinge not on how many genes you have, but what you do with them. As the authors of the current paper write, “the complexity of eukaryotes relative to bacteria and archaea is a consequence of the increased connectivity and plasticity of networks and interactions, rather than an increase in the amount of coding DNA”.
To test this idea, Nigel Goldenfeld, of the University of Illinois, and Thomas Kuhlman, a former physics professor at Illinois who is now at University of California, Riverside, decided to put this hypothesis to the test, by using Kuhlman’s own DNA.
Their results were a surprise.
“We thought a really simple thing to try was to just take one [retrotransposon] out of my genome and put it into the bacteria just to see what would happen,” says Kuhlman. “And it turned out to be really quite interesting.”
And by interesting, he means “fatal”.
“As they jump around and make copies of themselves, they jump into genes that the bacteria need to survive,” he says, “It's incredibly lethal to them.”
Which explains why they are so rare in bacteria.
To survive, organisms must repair the damage done by retrotransposons as they cut host DNA to insert themselves into the genome. Primitive repair mechanisms remove the invader, but eukaryotes can fix the DNA while preserving the added complexity brought by the jumping genes, a technique called nonhomologous end-joining, or NHEJ.
Goldenfeld, Kuhlman and colleagues thought that giving bacteria the ability to do NHEJ might help them cope with retrotransposon invasion.
They were wrong.
“It just completely killed everything,” says Kuhlman.
NHEJ, it turns out, actually improves the ability of retrotransposons to proliferate through the genome. This led the researchers to realise that the technique must play a central role in the action of transposable elements in eukaryotes and is thus far more important than anyone has realised to date.
With increased junk DNA comes a greater genetic repertoire which allows organisms to do more with the genes they have. Molecular machines called spliceomes, also evolved from bacterial group II introns and thus related to retrotransposons, , can cut the DNA in various ways to generate different functions and thus increased biological complexity.
Therefore, it seems that NHEJ in eukaryotes facilitated the proliferation of transposable elements, some of which evolved into retrotransposons and the spliceome. Together these form an engine that produced increased genetic complexity, without an increase in the amount of coding DNA, which in turn enabled the elevated biological complexity we see in plants, animals and fungi today.