Junk DNA, or more scientifically, transposable elements (TE's) have been known for many years to move back and forth within genomes. The theory that TE activity is induced by environmental and population factors is not new either (link). But the underlying mechanisms behind how this activity is affected by stress remains hypothesised, as does how the host genome controls transposition (movement of TE's).
Often the movement of TE's can have negative dramatic effects. However transposition can also be advantageous and enhance survival by activating or forming new genes. Why else would the benefits of transposition exist other than to mediate the interaction between genome and environment?
Many studies have been completed involving TE's in Drosophila fruit flies and various plants but it is the humble bacteria Escherichia coli (E. coli) that has revealed new links between transposition, cellular stress to the host genome, and regulation of TE movement.
Twiss et al. (2005) found that in response to nutritional stress of E. coli, transposition is likely to be favoured and even induced. In such situations gene rearrangements were critical to cell survival. It was found also that hosts can regulate transposition using a variety of proteins during stress-inducing situations so that a balance between the deleterious effects of transposition and the potential useful outcomes of genome rearrangement can occur.
TE's are the major internal spontaneous mutation agents for the variability of genomes. Stress activated TE's generate the raw diversity that a species requires over evolutionary time to survive specific stresses. In relation to the human race and evolution, is stress such a bad thing after all?
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