Figure 1:

An integrated model of stress-induced retrotransposon (re)activation and the allostatic load concept. Exogenous and endogenous challenges increase the allostatic load on the body, which represents an average allostatic load experienced by all cells in the organism. A consequence of this is that not all cells will experience higher allostatic load following stress; some might even experience less allostatic load. High cellular allostatic load leads to loss of epigenetic silencing in heterochromatic genomic regions, which is followed by (re)activation of retrotransposons. Losing control of retrotransposons has different consequences and tradeoffs depending on cell type. In somatic cells, it may help an individual animal to generate cellular diversity important for normal development, but may also cause genome instability which may increase the risk of disease. In germ cells, retrotransposon (re)activation may cause infertility, but also contribute to species evolvability by increasing genetic diversity. Hypothetically, a challenging environment could, by increasing the allostatic load, induce the genome-wide transposon amplification events observed in most eukaryotes, thereby representing a tool for a population/species to adapt to the challenging environment.