By Yassi Khorsandian
Even though over half of our genome consists of jumping genes, little is known about their functionality and how cells have adapted to survive from their invasions. Since their discovery in 1983, these genes that are now more commonly referred to as transposons, have been found to trigger mutations in the DNA, resulting in sterility or death. A team of researchers at the Carnegie Institution have discovered a novel ability of stem cells to increase the production of non-coding RNAs that decrease the activity of these genes. They studied transposons under different temperature settings in the fruit fly Drosophila melanogaster because temperature has been proven to affect the sterility of these organisms. The results showed that the rate of transposon mobilization was seven times greater at 25° C, the temperature at which the fruit fly offspring are sterile. The search for the underlying adaptive mechanism that causes this reaction led them to a DNA checkpoint component named Chk2, which was found to be the main constituent of the stem cell response to the transposon invasion. Activating this DNA damage checkpoint momentarily pauses the cell cycle before cell division in order to repair the damaged genome. This interruption in the cell cycle also boosts the production of piRNA elements that suppress transposons, allowing fruit flies to resume normal egg production. This pause period has proven to be critical for increasing the organism’s adaptability and counteracting the genomic instability caused by jumping genes.
Carnegie Institution for Science. (2018, November 1). How invading jumping genes are thwarted. ScienceDaily. Retrieved November 12, 2018 from www.sciencedaily.com/releases/2018/11/181101133942.htm