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Molecular and Cellular Biology, July 2007, p. 4991-5001, Vol. 27, No. 13
0270-7306/07/$08.00+0     doi:10.1128/MCB.00515-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Transcriptional Activity of the Telomeric Retrotransposon HeT-A in Drosophila melanogaster Is Stimulated as a Consequence of Subterminal Deficiencies at Homologous and Nonhomologous Telomeres

Radmila Capkova Frydrychova,¹ Harald Biessmann,² Alexander Y. Konev,^1, Mikhail D. Golubovsky,^1, Jessica Johnson,¹ Trevor K. Archer,³ and James M. Mason^1*

Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709,¹ Developmental Biology Center, University of California, Irvine, California 92697,² Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709³

Received 24 March 2007/ Accepted 13 April 2007

Drosophila melanogaster telomeres have two DNA domains: a terminal array of retrotransposons and a subterminal repetitive telomere-associated sequence (TAS), a source of telomere position effect (TPE). We reported previously that deletion of the 2L TAS array leads to dominant suppression of TPE by stimulating in trans expression of a telomeric transgene. Here, we compared the transcript activities of a w transgene inserted between the retrotransposon and TAS arrays at the 2L telomere in genotypes with different lengths of the 2L TAS. In contrast to individuals bearing a wild-type 2L homologue, flies with a TAS deficiency showed a significant increase in the level of telomeric w transcript during development, especially in pupae. Moreover, we identified a read-through w transcript initiated from a retrotransposon promoter in the terminal array. Read-through transcript levels also significantly increased with the presence of a 2L TAS deficiency in trans, indicating a stimulating force of the TAS deficiency on retrotransposon promoter activity. The read-through transcript contributes to total w transcript, although most w transcript originates at the w promoter. While silencing of transgenes in nonhomologous telomeres is suppressed by 2L TAS deficiencies, suggesting a global effect, the overall level of HeT-A transcripts is not increased under similar conditions.

Published ahead of print on 30 April 2007.

Present address: Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY.

Present address: Center for Demographic Studies, Duke University, Durham, NC.

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