By recombination, but this passive process may turn out to be
By recombination, but this passive process may turn out to be less efficient than transposition. Second, the genome may inactivate TEs through targeted mutations. Such a process has been described in Neurospora crassa and other fungi, and is known as RIP (Repeat-Induced-Point mutations). It is quite efficient, at least in N. crassa, in the genome of which no intact TEs or TE activity can be detected [131]. The drawbacks are that the genome loses the benefits of TEs as a source of variations, and the benefits of having multigenic families – although in some conditions RIP may accelerate allele evolution [132]. Third, the genome may silence TEs epigenetically without destroying them. This is an efficient process, and one that has the advantage of being both transmissible and reversible. The potential source of variability (TEs) is still present in an inactivated state, but may occasionally be reactivated. Bursts of amplifications seem to have repeatedly occurred in the history of some genomes, and reflect periods when TEs escaped from epigeneticThe contribution of transposable elements to the epigenetic phenomenon has recently been unraveled, but had long been suspected since McClintock proposed the existence of controlling elements as a response to environmental (or genomic) stresses [79]. From anecdotal “disturbers”, TEs have now moved centre-stage and revealed to contribute to genome regulation and genome robustness and/or evolvability [68,134]. Transposable elements seem to occur in regions in which a concentration of epigenetic landmarks can be observed, and are often the target of the epigenetic control [68]. This may have two impacts: first, TE silencing; second, modification of the expression profile of nearby genes. While TE silencing will avoid PM01183MedChemExpress Lurbinectedin amplification bursts, thus promoting a degree of stability, the silencing of genes in their vicinity may have an impact on the host [135]. More intriguingly, there are numerous examples suggesting the implication of TEs in the normal epigenetic regulation of genes, including genes involved in various developmental processes [68,109,136]. The assumption that TEs also contribute to regulation via intrinsic regulatory properties through nucleosome binding and phasing, epigenetic enhancers and boundary elements [137] constitutes a further step. Finally, TEs may have been exapted for these regulatory properties. Few PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27735993 studies have focused on histone modifications at TE sites, and the relationship between them remains poorly understood. In mammals, different TE classes seem to be targets for different histone modifications. However, contradictory findings make it difficult to work out whether histone modifications at TE sites result from a genomic defense or from exaptation for the regulation of adjacent genes [113]. It has long been known that a number of elements seems to reactivate following various stresses [138-140], and stress responses of retroelements are well documented in plants [141]. In Capy et al. [142], it was assumed that environmental changes can directly affect TE activity through the fixation of transcription activators onHua-Van et al. Biology Direct 2011, 6:19 http://www.biology-direct.com/content/6/1/Page 11 ofthe regulatory region of the elements. It is now clear that TE reactivation by stress or environmental changes usually involves epigenetic changes [107]. Since the epigenetic state of TEs also influences the expression of adjacent genes, the reaction of the genome to st.