A genetically tagged, defective I element can be complemented by actively transposing I factors in the germaine of I-R dysgenic females inDrosophila melanogaster

Abstract

Non-LTR retrotransposons, also known as LINEs, transpose by reverse transcription of an RNA intermediate. Their mechanism of transposition is apparently different from that of retrotransposons and similar to that of proviruses of retroviruses. The I factor is responsible for the I-R system of hybrid dysgenesis in Drosophila melanogaster. Inducer strains contain several functional I factors whereas reactive strains do not. Transposition of I factors can be experimentally induced: they are stable in inducer strains, but transpose at high frequency in the germline of females, known as SF females, produced by crossing reactive females and inducer males. We have constructed an I element, called IviP2, marked with the vermilion gene, the coding sequence of which was interrupted by an intron. Splicing of the intron can only occur in the transcript initiated from the I element promoter. Transposed copies expressing a wild-type vermilion phenotype were recovered in the germline of SF females in which I factors were actively transposing. This indicates that trans-complementation of a defective I element, deficient for the second open reading frame, by functional I factors can occur in the germline of dysgenic females.

Evidence for recent horizontal transfer of gypsy-homologous LTR-retrotransposon gtwin into Drosophila erecta followed by its amplification with multiple aberrations

“…It is possible that the number of copies with deletions appeared as the result of reverse transcription of partially degraded RNA. It is interesting that a similar phenomenon was demonstrated for I-element (Pelisson et al, 1991;Chaboissier et al, 1995). …”

Boudicca , a Retrovirus-Like Long Terminal Repeat Retrotransposon from the Genome of the Human Blood Fluke Schistosoma mansoni

“…Verification that the consensus Boudicca represents an ostensibly active retrotransposon may have to await the generation of the entire genome sequence of S. mansoni, a task that is now claiming the attention of a number of genome sequencing labs (24). Ret- rotransposons with degraded sequences may also be capable of functioning to a limited extent, since one copy can be transcribed and reinserted with functional proteins produced by another copy by a process of transcomplementation (2,9,65).…”

Population dynamics of PIWI-interacting RNAs (piRNAs) and their targets in Drosophila

“…Various mechanisms of repression of TE activities have been incorporated into our understanding of the population genetics of TEs, including self-regulation of copy number by reducing transposition rates (Charlesworth and Charlesworth 1983;Langley et al 1983), cis-acting regulation (transposition immunity) and trans-acting regulation (transposition repression) of TEs (Charlesworth and Langley 1986), regulation of transposition by host factors (Badge and Brookfield 1998), or more specifically, regulation of transposition by the interaction between TEs and the host genome such as the P-M hybrid dysgenesis system (Engels 1986;Boussy et al 1988;Brookfield 1991;Coen et al 1994;Anxolabehere 1997, 1998) or the I-R hybrid dysgenesis system (Proust et al 1992;Chaboissier et al 1995;Jensen et al 1995Jensen et al , 2002. Recently, it was discovered that PIWI-interacting RNAs (piRNAs), a class of small (26-31 bp) RNA molecules, are crucial repressors of active TEs in the germlines of fruit flies and worms (Aravin et al 2001Nishida and Siomi 2006;Vagin et al 2006;Brennecke et al 2007Brennecke et al , 2008Nishida et al 2007;Yin and Lin 2007;Das et al 2008;Ghildiyal et al 2008;Girard and Hannon 2008;Siomi and Siomi 2008;Li et al 2009;).…”