Abstract
Mutator-like transposable elements (MULEs) are widespread in plants and the majority have long terminal inverted repeats (TIRs), which distinguish them from other DNA transposons. It is known that the long TIRs of Mutator elements harbor transposase binding sites and promoters for transcription, indicating that the TIR sequence is critical for transposition and for expression of sequences between the TIRs. Here, we report the presence of MULEs with multiple TIRs mostly located in tandem. These elements are detected in the genomes of maize, tomato, rice, and Arabidopsis. Some of these elements are present in multiple copies, suggesting their mobility. For those elements that have amplified, sequence conservation was observed for both of the tandem TIRs. For one MULE family carrying a gene fragment, the elements with tandem TIRs are more prevalent than their counterparts with a single TIR. The successful amplification of this particular MULE demonstrates that MULEs with tandem TIRs are functional in both transposition and duplication of gene sequences.
Highlights
Transposable elements (TEs) are DNA fragments that are capable of moving from one genomic location to another and increasing their copy numbers
A typical Mutator-like transposable elements (MULEs) contains one pair of terminal inverted repeats (TIRs), which refers to similar or identical terminal inverted sequences found on the opposite ends of the element (Figure 1, see above)
We detected some atypical MULEs with two pairs of TIRs, which will be referred to as external TIR and internal TIR, respectively
Summary
Transposable elements (TEs) are DNA fragments that are capable of moving from one genomic location to another and increasing their copy numbers. It was shown that the transposase of the Hermes element binds to its imperfect TIRs and excises the element. This process is accompanied by the formation of a hairpin structure in the flanking donor sequence, resembling the V(D)J recombination process [2]. Binding of transposase to the TIR and to the target DNA mediates the synapsis of the transposon ends and the target DNA, allowing the insertion of the element into the target sequence [3]. The deletion of a 4 bp sequence within the binding region of the TIR in Tn3 abolishes its transposition immunity, that is, the phenomenon whereby Tn3 avoids insertion into another Tn3 element [4]
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