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Viruses 2017, 9(4), 81;

Mechanisms of LTR‐Retroelement Transposition: Lessons from Drosophila melanogaster

Department of Biology, Moscow State University, Moscow 119992, Russia
Author to whom correspondence should be addressed.
Academic Editors: David J. Garfinkel and Katarzyna J. Purzycka
Received: 31 January 2017 / Revised: 6 April 2017 / Accepted: 10 April 2017 / Published: 16 April 2017
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Long terminal repeat (LTR) retrotransposons occupy a special place among all mobile genetic element families. The structure of LTR retrotransposons that have three open reading frames is identical to DNA forms of retroviruses that are integrated into the host genome. Several lines of evidence suggest that LTR retrotransposons share a common ancestry with retroviruses and thus are highly relevant to understanding mechanisms of transposition. Drosophila melanogaster is an exceptionally convenient model for studying the mechanisms of retrotransposon movement because many such elements in its genome are transpositionally active. Moreover, two LTRretrotransposons of D. melanogaster, gypsy and ZAM, have been found to have infectious properties and have been classified as errantiviruses. Despite numerous studies focusing on retroviral integration process, there is still no clear understanding of integration specificity in a target site. Most LTR retrotransposons non‐specifically integrate into a target site. Site‐specificity of integration at vertebrate retroviruses is rather relative. At the same time, sequence‐specific integration is the exclusive property of errantiviruses and their derivatives with two open reading frames. The possible basis for the errantivirus integration specificity is discussed in the present review. View Full-Text
Keywords: Drosophila; LTR‐retrotransposon; errantivirus; retrovirus; transposition Drosophila; LTR‐retrotransposon; errantivirus; retrovirus; transposition

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Nefedova, L.; Kim, A. Mechanisms of LTR‐Retroelement Transposition: Lessons from Drosophila melanogaster. Viruses 2017, 9, 81.

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