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Natural epigenetic protection against the I-factor, a Drosophila LINE retrotransposon, by remnants of ancestral invasions.

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.

SUBMITTER: Dramard X

PROVIDER: S-EPMC1810428 | biostudies-literature | 2007

REPOSITORIES: biostudies-literature

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Natural epigenetic protection against the I-factor, a Drosophila LINE retrotransposon, by remnants of ancestral invasions.

Dramard Xavier X Heidmann Thierry T Jensen Silke S

PloS one 20070321 3

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 ...[more]

PMID: 17375190

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Project description:Analysis of terminal deletion chromosomes indicates that a sequence-independent mechanism regulates protection of Drosophila telomeres. Mutations in Drosophila DNA damage response genes such as atm/tefu, mre11, or rad50 disrupt telomere protection and localization of the telomere-associated proteins HP1 and HOAP, suggesting that recognition of chromosome ends contributes to telomere protection. However, the partial telomere protection phenotype of these mutations limits the ability to test if they act in the epigenetic telomere protection mechanism. We examined the roles of the Drosophila atm and atr-atrip DNA damage response pathways and the nbs homolog in DNA damage responses and telomere protection. As in other organisms, the atm and atr-atrip pathways act in parallel to promote telomere protection. Cells lacking both pathways exhibit severe defects in telomere protection and fail to localize the protection protein HOAP to telomeres. Drosophila nbs is required for both atm- and atr-dependent DNA damage responses and acts in these pathways during DNA repair. The telomere fusion phenotype of nbs is consistent with defects in each of these activities. Cells defective in both the atm and atr pathways were used to examine if DNA damage response pathways regulate telomere protection without affecting telomere specific sequences. In these cells, chromosome fusion sites retain telomere-specific sequences, demonstrating that loss of these sequences is not responsible for loss of protection. Furthermore, terminally deleted chromosomes also fuse in these cells, directly implicating DNA damage response pathways in the epigenetic protection of telomeres. We propose that recognition of chromosome ends and recruitment of HP1 and HOAP by DNA damage response proteins is essential for the epigenetic protection of Drosophila telomeres. Given the conserved roles of DNA damage response proteins in telomere function, related mechanisms may act at the telomeres of other organisms.

Dataset Information

Natural epigenetic protection against the I-factor, a Drosophila LINE retrotransposon, by remnants of ancestral invasions.

Publications

Natural epigenetic protection against the I-factor, a Drosophila LINE retrotransposon, by remnants of ancestral invasions.

Similar Datasets

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