Abstract
The molecular mechanisms of the transposition of non-long terminal repeat (non-LTR) retrotransposons are not well understood; the key questions of how the 3′-ends of cDNA copies integrate and how site-specific integration occurs remain unresolved. Integration depends on properties of the endonuclease (EN) domain of retrotransposons. Using the EN domain of the Drosophila R2 retrotransposon as a model for other, closely related non-LTR retrotransposons, we investigated the EN domain and found that it resembles archaeal Holliday-junction resolvases. We suggest that these non-LTR retrotransposons are co-transcribed with the host transcript. Combined with the proposed resolvase activity of the EN domain, this model yields a novel mechanism for site-specific retrotransposition within this class of retrotransposons, with resolution proceeding via a Holliday junction intermediate.
Highlights
Eukaryotic transposable elements (TEs) are ubiquitous components of eukaryotic genomes that are important for shaping the genetic material
Given that the position of the second nick in relation to that of the first nick varies in different groups of TE, we propose two possible schemes for the transposition process: the first one applies to transpositions with deletion of the target site, and the second one applies to transpositions with duplication of the target site
On the basis of the experimental evidence that R2 EN is highly sequence-specific to its target site on double-stranded DNA and can cleave single-stranded DNA (ssDNA) that extends from the ends of the dsDNA region (Kurzynska-Kokorniak et al, 2007), we propose that the protein www.frontiersin.org that makes the first DNA nick will move to the end of the dsDNA helix after a complementary DNA strand is synthesized
Summary
Eukaryotic transposable elements (TEs) are ubiquitous components of eukaryotic genomes that are important for shaping the genetic material. New copies of TEs integrate into new sites in the genome and can cause genomic and genetic variations. New insertions can: (1) alter gene expression by providing cis-regulatory elements, such as promoters, enhancers, and transcription factor binding sites; (2) induce insertion-mediated deletions; or (3) affect chromosome replication, recombination, and pairing. The spread of regulatory elements by TEs can lead to the creation of specific regulatory networks, induce pathologies including cancer, affect host environmental adaptations, or contribute to genetic diversity. TEs have a large impact on genome evolution (for review, see Oliver and Greene, 2009; Bire and Rouleux-Bonnin, 2012; Kim et al, 2012; Casacuberta and González, 2013; Chénais, 2013). Understanding the mechanisms of TE dissemination, in particular, the mechanism of transposition, is of great general importance
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