Mechanisms of LTR‐Retroelement Transposition: Lessons from Drosophila melanogaster

Abstract

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 LTR-retrotransposons 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.

Diversification and collapse of a telomere elongation mechanism

“…These non-autonomous elements are found both inside and outside the D. biarmipes telomeres (Fig. 4D) and found more typically outside the telomere in other Drosophila species (Kas and Laemmli 1992; Kapitonov and Jurka 2007; Nefedova and Kim 2017). Moreover, we found not one full-length Helitron in the D. biarmipes genome, rejecting the possibility of contemporary propagation using mobilization proteins in trans (Fig.…”

“…If newly domesticated mobile elements readily replace ancestral, telomere-specialized lineages, we would expect the species ostensibly lacking active jockey subclade elements— D. biarmipes —to encode such new recruits. The extreme terminal ends of D. biarmipes instead harbor AT-rich satellite “SAR” DNA (Mirkovitch et al 1984; Kas and Laemmli 1992) at all telomeres as well as Helitron fragments (Kapitonov and Jurka 2007) and Gypsy-derived LTR fragments (Nefedova and Kim 2017) at variable frequencies across different telomeres. These non-autonomous elements are found both inside and outside the D. biarmipes telomeres (Fig.…”

Diversification and collapse of a telomere elongation mechanism

“…If newly domesticated mobile elements readily replace ancestral, telomere-specialized lineages, we would expect the species lacking active jockey subclade elements-D. biarmipes-to encode such new recruits. The extreme terminal ends of D. biarmipes instead harbor AT-rich satellite "SAR" DNA (Mirkovitch et al 1984;Käs and Laemmli 1992) at all telomeres, as well as Helitron fragments (Kapitonov and Jurka 2007) fragments (Nefedova and Kim 2017) at variable frequencies across different telomeres. These inactive elements are found both inside and outside the D. biarmipes telomeres (Fig.…”

Retrotransposons Manipulating Mammalian Skeletal Development in Chondrocytes

“…Particularly, considering their extraordinary genome occupancy, no humans with present shape, which is determined mostly by endochondral ossification, were present without HERV, LINEs, and SINEs. In addition, the fact that the genomes of crustacean and insects contain a number of retrotransposons suggests their contribution to intramembranous ossification-the older form of bone formation [97,98]. Thus, retrotransposons may be manipulating our craniofacial development by directly regulating osteoblasts as well.…”