Reactive strains lack such functional elements because they had been sequestered in laboratories before the recent invasion mentioned above. Under normal conditions, these functional copies do not transpose at a detectable rate. Inducer strains contain transpositionally competent I-factors, initially acquired following an invasion of wild flies in the course of the twentieth century. With respect to I-factors, all Drosophila melanogaster strains fall into two categories named “inducer” and “reactive”. The I-factor transposes in a replicative manner, through the reverse transcription of its full-length RNA, , which encodes the proteins necessary for its mobility. The Drosophila I-factor (FlyBase GeneID number FBGn0001249) belongs to the LINE (Long Interspersed Nucleotidic Element) superfamily, which represents the major class of transposable elements in mammals (about 20% of the human genome). The molecular mechanisms involved in this “taming” process are far from being understood, but there is strong evidence that RNA interference (RNAi) – affects the activity of several mobile elements –, notably in Drosophila (reviewed in reference ). The copies of mobile elements that remain functional are severely repressed by their host, possibly as a biological requisite for genomic stability of species and individuals, since high levels of transposition would result in the accumulation of detrimental insertional mutations and genome rearrangements. They are now stable components of the genomes. Most of these sequences have lost their ability to transpose.
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In the course of evolution, transposable elements have accumulated in the genome of eukaryotes, where they can account for up to 80% of the DNA. These results provide a molecular basis for a probably widespread natural protection against transposable elements by persisting vestiges of ancient invasions. 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. 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. However, this high transpositional activity becomes spontaneously repressed upon ageing or heat treatment, by a maternally transmitted, transgenerational epigenetic mechanism of unknown nature. 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. Drosophila pericentromeric heterochromatin naturally contains transposition-defective, non-coding derivatives of a LINE retrotransposon related to the I-factor. Because transposition can be highly mutagenic, mobile elements that remain functional are tightly repressed in all living species. Such sequences are generally defective for transposition and have little or no coding capacity. Transposable elements are major components of most eukaryotic genomes.
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