Abstract
Background Mariner elements represent the most successful family of autonomous DNA transposons, being present in various plant and animal genomes, including humans. The introduction and co-evolution of mariners within host genomes imply a strict regulation of the transposon activity. Biochemical data accumulated during the past decade have led to a convergent picture of the transposition cycle of mariner elements, suggesting that mariner transposition does not rely on host-specific factors. This model does not account for differences of transposition efficiency in human cells between mariners. We thus wondered whether apparent similarities in transposition cycle could hide differences in the intrinsic parameters that control mariner transposition.Principal FindingsWe find that Mos1 transposase concentrations in excess to the Mos1 ends prevent the paired-end complex assembly. However, we observe that Mos1 transposition is not impaired by transposase high concentration, dismissing the idea that transposase over production plays an obligatory role in the down-regulation of mariner transposition. Our main finding is that the paired-end complex is formed in a cooperative way, regardless of the transposase concentration. We also show that an element framed by two identical ITRs (Inverted Terminal Repeats) is more efficient in driving transposition than an element framed by two different ITRs (i.e. the natural Mos1 copy), the latter being more sensitive to transposase concentration variations. Finally, we show that the current Mos1 ITRs correspond to the ancestral ones.ConclusionsWe provide new insights on intrinsic properties supporting the self-regulation of the Mos1 element. These properties (transposase specific activity, aggregation, ITR sequences, transposase concentration/transposon copy number ratio…) could have played a role in the dynamics of host-genomes invasion by Mos1, accounting (at least in part) for the current low copy number of Mos1 within host genomes.
Highlights
Transposable elements make up the largest fraction of many eukaryotic genomes [1]
We investigated the importance of the transposase (MOS1) concentration in the paired-end complex (PEC) assembly
We subsequently showed that Mos1 transposition was initiated by the binding of one transposase dimer at one inverted terminal repeats (ITRs) [15]
Summary
Transposable elements make up the largest fraction of many eukaryotic genomes [1]. Among them, mariner elements represent one of the most widespread groups of DNA transposons. The mariner elements life cycle depends on frequent horizontal transfer into new hosts. Mariner elements represent the most successful family of autonomous DNA transposons, being present in various plant and animal genomes, including humans. Biochemical data accumulated during the past decade have led to a convergent picture of the transposition cycle of mariner elements, suggesting that mariner transposition does not rely on host-specific factors. This model does not account for differences of transposition efficiency in human cells between mariners. We wondered whether apparent similarities in transposition cycle could hide differences in the intrinsic parameters that control mariner transposition
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