Genomic parasites

Genomic parasites – we all have them but how are they kept under control?

You may think you are parasite free. “No malaria, bilharzia or tapeworms in me”, I hear you say… If you think this you’re actually mistaken. Humans, and many organisms besides, carry parasites within their own DNA. These parasites have left behind the ‘traditional’ parasitic life cycle, with their own body or their own cell living within us and have gone purist, trimming everything away and simply copying their genome into ours, existing alongside us for as long as humans survive. Known as transposons, these genomic parasites use our own cells to survive, using our own machinery to copy themselves, replicating and surviving just as organisms endeavour to do on the land, in the air or in the sea. They could copy themselves all over our genome making even more copies of themselves but something prevents this, stopping the transposon from overwhelming our genome and killing us. Research from the University of Cambridge, the University of Nottingham, and the Fred Hutchinson Cancer Centre in Seattle reveals why:

Transposase is important to the genetic “jump” of transposons because it catalyses 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 found 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.

See more on the Cambridge University research page and read the paper from eLife:

Bouuaert et al., 2013, The autoregulation of a eukaryotic DNA transposon, eLife

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