Figure 1. Transposition of class I and class II elements results in the integration of a DNA sequence into a new host acceptor site. Class I elements propagate via an RNA intermediate which is reverse transcribed into DNA. Class II elements transpose via a ‘cut-and-paste’ mechanism which is indicated by the two arrows at the borders of the elements.

Figure 2. Class I: Ty1 in yeast (LTR retrotransposon). Ty1 is bordered by retroviral long terminal repeats (LTRs). Two reading frames encode a coat protein (gag), a protease (prot), the integrase (int) and the reverse transcriptase (RT). The host DNA sequence shows small target site duplications (TSDs), which are indicated by the red arrows outside the LTRs. After reverse transcription the DNA intermediate is integrated by integrase activity. The resulting gaps are filled in by host DNA repair enzymes. Thus TSDs are generated.

Figure 3. Class I: LINEs and SINEs (non-LTR retrotransposons). A hypothetical transposition model for non-LTR retrotransposons is shown for LINEs and SINEs. Pol II and pol III are the promotor sequences that allow transcription of the elements. LINEs comprise two reading frames which encode for the coat protein (gag), the endonuclease (EN) and the reverse transcriptase (RT). After transcription, integration is started via RNA invasion. The first strand synthesis is mediated by the free 3¢-hydroxyl group in the host DNA as a primer. The second strand synthesis is primed by the opposite strand of the host DNA. Varying target site duplications after transposition are indicated by nested triangles.

Figure 4. Class II: Ac in maize (DNA transposable elements). The centrally located ORFa, marked by red bars, encodes for the transposase (TPase). This protein recognizes the 11-bp terminal inverted repeats (TIRs) and multiple subterminal binding sites (indicated by red dots). The 8-bp target site duplications (TSDs) at the ends (outside) of the TIRs are marked by red arrows. In the hypothetical transposon (a DNA–protein complex necessary for transposition) the termini are tethered by TPase molecules. The binding to the TIRs results in blunt-end cuts directly at the border outside the TIRs. The new acceptor site reveals staggered nicks. After transposition, TSDs can be observed as footprints at the empty donor site. The gaps at the acceptor site are filled in by the host repair machinery.

Figure 5. Antirrhinum majus flower. A pallida recurrens line with the active and temperature-sensitive Tam3 element at the pallida locus. Each dot of the variegation means that a transposon has left the locus and wild-type function of anthocyanin biosynthesis is restored. The earlier the event, the more extensive the resulting cell line and the larger the restored anthocyanin patch. Photograph by Maret Kalda, MPI, Cologne.

Figure 6. Class II: P in Drosophila melanogaster (DNA transposable element). P-element transposition is regulated by alternative splicing. Only in germline cells is intron 3 spliced out. Hence, the central coding sequence marked by red bars leads to transcripts of different sizes, which correspond to ORFs of different lengths. A 66-kDa repressor of transposition is translated in somatic cells. In contrast, an 87-kDa transposase is translated in germline cells. The TPase DNA-binding positions are indicated by red dots within the element. The target site duplications are marked just outside of the element by red arrows.