Editing Transposable element (section)

== Rate of transposition, induction and defense ==
One study estimated the rate of transposition of a particular retrotransposon, the [[Ty1]] element in ''[[Saccharomyces cerevisiae]]''. Using several assumptions, the rate of successful transposition event per single Ty1 element came out to be about once every few months to once every few years.<ref>{{cite journal | vauthors = Paquin CE, Williamson VM | s2cid = 39145808 | title = Temperature effects on the rate of ty transposition | journal = Science | volume = 226 | issue = 4670 | pages = 53–5 | date = October 1984 | pmid = 17815421 | doi = 10.1126/science.226.4670.53 | bibcode = 1984Sci...226...53P }}</ref> Some TEs contain [[Heat shock protein|heat-shock like]] promoters and their rate of transposition increases if the cell is subjected to stress,<ref>{{cite journal | vauthors = Strand DJ, McDonald JF | title = Copia is transcriptionally responsive to environmental stress | journal = Nucleic Acids Research | volume = 13 | issue = 12 | pages = 4401–10 | date = June 1985 | pmid = 2409535 | pmc = 321795 | doi = 10.1093/nar/13.12.4401 }}</ref> thus increasing the mutation rate under these conditions, which might be beneficial to the cell.

Cells defend against the proliferation of TEs in a number of ways. These include [[Piwi-interacting RNA|piRNA]]s and [[siRNA]]s,<ref>{{cite journal | vauthors = Chung WJ, Okamura K, Martin R, Lai EC | title = Endogenous RNA interference provides a somatic defense against Drosophila transposons | journal = Current Biology | volume = 18 | issue = 11 | pages = 795–802 | date = June 2008 | pmid = 18501606 | pmc = 2812477 | doi = 10.1016/j.cub.2008.05.006 | bibcode = 2008CBio...18..795C }}</ref> which [[gene silencing|silence]] TEs after they have been transcribed.

If organisms are mostly composed of TEs, one might assume that disease caused by misplaced TEs is very common, but in most cases TEs are silenced through [[epigenetics|epigenetic]] mechanisms like [[DNA methylation]], chromatin remodeling and piRNA, such that little to no phenotypic effects nor movements of TEs occur as in some wild-type plant TEs. Certain mutated plants have been found to have defects in methylation-related enzymes (methyl transferase) which cause the transcription of TEs, thus affecting the phenotype.<ref name="prayla"/><ref name="Mobilization of transposons by a mu">{{cite journal | vauthors = Miura A, Yonebayashi S, Watanabe K, Toyama T, Shimada H, Kakutani T | s2cid = 4429219 | title = Mobilization of transposons by a mutation abolishing full DNA methylation in Arabidopsis | journal = Nature | volume = 411 | issue = 6834 | pages = 212–4 | date = May 2001 | pmid = 11346800 | doi = 10.1038/35075612 | bibcode = 2001Natur.411..212M }}</ref>

One hypothesis suggests that only approximately 100 LINE1 related sequences are active, despite their sequences making up 17% of the human genome. In human cells, silencing of LINE1 sequences is triggered by an [[RNA interference]] (RNAi) mechanism. Surprisingly, the RNAi sequences are derived from the 5′ untranslated region (UTR) of the LINE1, a long terminal which repeats itself. Supposedly, the 5′ LINE1 UTR that codes for the sense promoter for LINE1 transcription also encodes the antisense promoter for the [[miRNA]] that becomes the substrate for siRNA production. Inhibition of the RNAi silencing mechanism in this region showed an increase in LINE1 transcription.<ref name="prayla"/><ref>{{cite journal | vauthors = Yang N, Kazazian HH | s2cid = 32601334 | title = L1 retrotransposition is suppressed by endogenously encoded small interfering RNAs in human cultured cells | journal = Nature Structural & Molecular Biology | volume = 13 | issue = 9 | pages = 763–71 | date = September 2006 | pmid = 16936727 | doi = 10.1038/nsmb1141 }}</ref>