ArticleMolecular & general genetics : MGG1995
A genetically tagged, defective I element can be complemented by actively transposing I factors in the germline of I-R dysgenic females in Drosophila melanogaster.
Article in Molecular & general genetics : MGG, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 14 citations in OpenAlex.
- P-elements strengthen reproductive isolation within the Drosophila simulans species complex.Evolution; international journal of organic evolution · 2021Article
- Population dynamics of PIWI-interacting RNAs (piRNAs) and their targets in Drosophila.Genome research · 2010Article
- In vivo RNA localization of I factor, a non-LTR retrotransposon, requires a cis-acting signal in ORF2 and ORF1 protein.Nucleic acids research · 2005Article
- Boudicca, a retrovirus-like long terminal repeat retrotransposon from the genome of the human blood fluke Schistosoma mansoni.Journal of virology · 2003Article
- New insights on homology-dependent silencing of I factor activity by transgenes containing ORF1 in Drosophila melanogaster.Genetics · 2000Article
- Article
- A genetically marked I element in Drosophila melanogaster can be mobilized when ORF2 is provided in trans.Genetics · 1998Article
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Authors and funding
4 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
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.
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