Biologists from Utrecht discovered that the nematode C. elegans keeps transposons in check with a sophisticated mechanism. Due to the mechanism, the transposons cannot make any of the proteins needed to jump through the DNA. In this manner the nematodes render the transposons virtually harmless. The dcr-1 gene seems to play a crucial role in the mechanism.
During the study, Sylvia Fischer also discovered how new transposons can arise. If a transposon jumps out of the DNA a hole remains in the DNA chain. The body's recovery mechanism uses a transposon further along the DNA as an example to repair the damage. However, the example to be copied sometimes changes during the copying process. This gives rise to a new transposon in the form of a hybrid of the chosen example.
In the future transposons could serve as tools for gene therapy. For this to be realised more must be known about the behaviour of transposons in the cell. Gene therapy is the addition of a piece of DNA to somebody who is ill due to a genetic defect. In gene therapy the transposon should add a good version of a defective gene to the DNA. The research from Utrecht shows that transposons can only jump well if they do not carry too large a piece of DNA.
Transposons form almost half of the human DNA. They are also termed junk DNA, as they probably have no function. Transposons are probably remnants of viruses from the past. In some aspects the AIDS virus is similar to a transposon.