Do transposons jump in the brain?
July 26, 2017
The shape and function of every cell in our body is determined by the amount and types of protein molecules that they produce. The building plan for each cell is stored in the DNA of the genome. This information is carefully copied and passed on to daughter cells during the reproduction, development and growth of all living organisms. Any changes (mutations) that occur in the DNA of each cell could potentially have devastating effects on the function of a cell. Surprisingly, a substantial portion of most animals’ DNA consists of so-called transposons, or ‘jumping genes’, many of which have ancient viral origin. These sections of the DNA have the potential to move or ‘jump’ into random locations throughout the DNA and they are therefore able to induce mutation. Previous studies have suggested that every single cell in our brains, and in some other parts of our body, might harbour several of these jumping genes that have moved to new locations in the DNA. However, detecting movement of jumping genes is difficult which has made this area of research controversial and hotly debated.
In a recent study published in eLife, Treiber and Waddell set out to map new locations of jumping genes in the DNA of cells in the brain of single fruit flies, hoping that lessons learned from these small insects would further understanding of jumping genes in the human brain. Changes to the DNA of cells in the fruit fly brain had previously been implicated in flies losing their memory when they age. If this is true, studying flies could even help explain how jumping genes might influence an animal’s behaviour.
Surprisingly, and maybe reassuringly, Treiber and Waddell found that jumping genes appear to be a lot less active than previously thought. But why had earlier studies reported high rates of gene jumping? It seems like the experimental process of preparing the DNA, where each single DNA molecule needs to be copied many times so that there is enough material to analyse, often wrongly joins together two bits of DNA that are normally not connected. When these joins occur close to a jumping gene they deceivingly make it look as if the gene has actually jumped. Treiber and Waddell found that many sites that people would previously have considered to be a new location of a jumping gene are actually just mistakes made when DNA fragments become incorrectly joined together when experimental samples are being prepared for analysis.
Treiber and Waddell also developed a new method that allowed them to quantify how often these artificial DNA joins occur in an experimental sample. Although this led them to conclude that gene jumping does not happen as frequently as previously thought it also provides the transposon research community with an important new tool that will hopefully help the development of new ways of detecting active jumping genes.
The full paper can be viewed here