Recognizing the enemy within: licensing RNA-guided genome defense

Trends Biochem Sci. 2014 Jan;39(1):25-34. doi: 10.1016/j.tibs.2013.10.003. Epub 2013 Nov 23.


How do cells distinguish normal genes from transposons? Although much has been learned about RNAi-related RNA silencing pathways responsible for genome defense, this fundamental question remains. The literature points to several classes of mechanisms. In some cases, double-stranded RNA (dsRNA) structures produced by transposon inverted repeats or antisense integration trigger endogenous small interfering RNA (siRNA) biogenesis. In other instances, DNA features associated with transposons--such as their unusual copy number, chromosomal arrangement, and/or chromatin environment--license RNA silencing. Finally, recent studies have identified improper transcript processing events, such as stalled pre-mRNA splicing, as signals for siRNA production. Thus, the suboptimal gene expression properties of selfish elements can enable their identification by RNA silencing pathways.

Keywords: PIWI-interacting RNA; RNAi; genome defense; small RNA; small interfering RNA; transposon.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • DNA Transposable Elements*
  • Genomic Instability
  • Humans
  • Mutagenesis, Insertional
  • RNA Interference*
  • RNA Splicing
  • RNA, Double-Stranded / genetics
  • RNA, Double-Stranded / metabolism
  • RNA, Small Interfering / genetics*


  • DNA Transposable Elements
  • RNA, Double-Stranded
  • RNA, Small Interfering