
Transcriptional Activity of the Telomeric Retrotransposon HeT-A in Drosophila melanogaster Is Stimulated as a Consequence of Subterminal Deficiencies at Homologous and Nonhomologous Telomeres
Author(s) -
Radmila Čapková Frydrychová,
Harald Biessmann,
Alexander Y. Konev,
M. D. Golubovsky,
Jessica Johnson,
Trevor Archer,
James Mason
Publication year - 2007
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.00515-07
Subject(s) - retrotransposon , biology , telomere , drosophila melanogaster , long terminal repeat , transgene , genetics , promoter , position effect , gene silencing , gene , microbiology and biotechnology , gene expression , transposable element , genome
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 the2 L TAS array leads to dominant suppression of TPE by stimulating intrans expression of a telomeric transgene. Here, we compared the transcript activities of aw transgene inserted between the retrotransposon and TAS arrays at the2 L telomere in genotypes with different lengths of the2 L TAS. In contrast to individuals bearing a wild-type2 L homologue, flies with a TAS deficiency showed a significant increase in the level of telomericw transcript during development, especially in pupae. Moreover, we identified a read-throughw transcript initiated from a retrotransposon promoter in the terminal array. Read-through transcript levels also significantly increased with the presence of a2 L TAS deficiency intrans , indicating a stimulating force of the TAS deficiency on retrotransposon promoter activity. The read-through transcript contributes to totalw transcript, although mostw transcript originates at thew promoter. While silencing of transgenes in nonhomologous telomeres is suppressed by2 L TAS deficiencies, suggesting a global effect, the overall level ofHeT-A transcripts is not increased under similar conditions.