Stress, transposons and genome evolution
It has been shown that in flies and plants mutations in the stress protein HSP90 induce a wide spectrum of heritable phenotypic variants. The interpretation was that HSP90 is a capacitor of morphological evolution and buffers pre-existing genetic variation that is not expressed and accumulates in neutral conditions. This stress-sensitive storage and release of genetic variation by HSP90 would favour adaptive evolution. However, our recent study has suggested a different explanation of these results (Specchia et al., 2010). It has been demonstrated that HSP90 is involved in repression of transcription and mobilization of transposable elements in germ cells by affecting piRNA biogenesis. The reduction of HSP90 causes stress response-like activation and transposition of mobile elements along with a wide range of phenotypic variants due to the transposon insertions to the corresponding genes. Intriguingly, it has also found that other mutations that impair piRNA biogenesis are capable to induce phenotypic variation. This further indicates that the expression of morphological variability could be related to the disruption of the piRNA silencing mechanism. So that, we proposed that, in general, the stress causes the activation of transposons that induce de novo gene mutations affecting development pathways.