Taming of transposable elements by homology-dependent gene silencing View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1999-02

AUTHORS

Silke Jensen, Marie-Pierre Gassama, Thierry Heidmann

ABSTRACT

Transposable elements can invade virgin genomes within a few generations, after which the elements are 'tamed' and retain only limited transpositional activity. Introduction of the I element, a transposon similar to mammalian LINE elements, into Drosophila melanogaster genomes devoid of such elements initially results in high-frequency transposition of the incoming transposon, high mutation rate, chromosomal nondisjunction and female sterility, a syndrome referred to as hybrid dysgenesis (for review, see refs 2-4); a related syndrome has also been described in mammals. High-frequency transposition is transient, as the number of I elements reaches a finite value and transposition ceases after approximately ten generations. It has been proposed that the I elements encode a factor that negatively regulates their own transcription, but evidence for such a mechanism is lacking. Using the hybrid dysgenesis syndrome in Drosophila as a model, we show here that transpositional activity of the I element can be repressed by prior introduction of transgenes expressing a small internal region of the I element. This autoregulation presents features characteristic of homology-dependent gene silencing, a process known as cosuppression. Repression does not require any translatable sequence, its severity correlates with transgene copy number and it develops in a generation-dependent manner via germline transmission of a silencing effector in females only. These results demonstrate that transposable elements are prone to and can be tamed by homology-dependent gene silencing, a process that may have emerged during the course of evolution as a specific defense mechanism against these elements. More... »

PAGES

ng0299_209

Journal

TITLE

Nature Genetics

ISSUE

2

VOLUME

21

Author Affiliations

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/5997

    DOI

    http://dx.doi.org/10.1038/5997

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1008532286

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/9988275


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