Abad et al., 1989, Proc. Natl. Acad. Sci. U.S.A. 86: 8887--8891

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Abad et al., 1989, Proc. Natl. Acad. Sci. U.S.A. 86: 8887--8891
FlyBase Identifier FBrf0050874
FlyBase URL http://flybase.org/reports/FBrf0050874.html
Publication Type paper
Publication Year 1989
PubMed ID 2554335
PubMed URL http://www.ncbi.nlm.nih.gov/pubmed/2554335


A long interspersed repetitive element -- the I factor of Drosophila teissieri -- is able to transpose in different Drosophila species.


Long interspersed repetitive elements (LINEs) are transposable elements present in many species. In mammals they are difficult to study because most of them are defective and their transposition frequency is low. The I factor of Drosophila melanogaster is a LINE element that is particularly interesting because its transposition occurs at high frequency during I-R hybrid dysgenesis. This phenomenon occurs when males from the class of inducer strains are crossed with females from the class of reactive strains. Inducer strains contain several complete 5.4-kilobase I factors at various sites on the chromosomal arms. Reactive strains are devoid of complete I factors. Many results indicate that active I factors have invaded the D. melanogaster genome recently. To study the evolutionary history of I elements, we have cloned and sequenced a potentially active I factor from Drosophila teissieri. It is flanked by a target-site duplication and terminates at the 3' end by tandem repeats of the sequence TAA. When introduced into the germ line of a reactive strain of D. melanogaster by P element-mediated transformation, it is able to transpose and induces hybrid dysgenesis. This strengthens the hypothesis of a recent reinvasion of the D. melanogaster genome by active I factors giving rise to the inducer strains. They could have originated by horizontal transfer from another species. Such events also could occur for other LINE elements and might explain the spread of new variants in mammalian genomes. Moreover, the results give a further insight into I factor functional organization.

Genes from Reference

Gene(s) Dmel\w
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