ArticlePloS one2007
Natural epigenetic protection against the I-factor, a Drosophila LINE retrotransposon, by remnants of ancestral invasions.
Article in PloS one, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- Natural variation of piRNA expression affects immunity to transposable elements.PLoS genetics · 2017Article
- De novo piRNA cluster formation in the Drosophila germ line triggered by transgenes containing a transcribed transposon fragment.Nucleic acids research · 2013Article
- Retrotransposon-induced heterochromatin spreading in the mouse revealed by insertional polymorphisms.PLoS genetics · 2011Article
- How many antiviral small interfering RNAs may be encoded by the mammalian genomes?Biology direct · 2010Article
- Article
- Epigenetic transmission of piRNAs through the female germline.Genome biology · 2009Review
- An epigenetic role for maternally inherited piRNAs in transposon silencing.Science (New York, N.Y.) · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transposable elements are major components of most eukaryotic genomes. Such sequences are generally defective for transposition and have little or no coding capacity. Because transposition can be highly mutagenic, mobile elements that remain functional are tightly repressed in all living species. Drosophila pericentromeric heterochromatin naturally contains transposition-defective, non-coding derivatives of a LINE retrotransposon related to the I-factor. The I-factor is a good model to study the regulation of transposition in vivo because, under specific conditions, current functional copies of this mobile element can transpose at high frequency, specifically in female germ cells, with deleterious effects including female sterility. However, this high transpositional activity becomes spontaneously repressed upon ageing or heat treatment, by a maternally transmitted, transgenerational epigenetic mechanism of unknown nature. We have analyzed, by quantitative real time RT-PCR, the RNA profile of the transposition-defective I-related sequences, in the Drosophila ovary during ageing and upon heat treatment, and also in female somatic tissues and in males, which are not permissive for I-factor transposition. We found evidence for a role of transcripts from these ancestral remnants in the natural epigenetic protection of the Drosophila melanogaster genome against the deleterious effects of new invasions by functional I-factors. These results provide a molecular basis for a probably widespread natural protection against transposable elements by persisting vestiges of ancient invasions.
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