Transcriptional activity of the telomeric retrotransposon HeT-A in Drosophila melanogaster is stimulated as a consequence of subterminal deficiencies at homologous and nonhomologous telomeres.

Transcriptional activity of the telomeric retrotransposon HeT-A in Drosophila melanogaster is stimulated as a consequence of subterminal deficiencies at homologous and nonhomologous telomeres. Research Abstract Details 

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Transcriptional activity of the telomeric retrotransposon HeT-A in Drosophila melanogaster is stimulated as a consequence of subterminal deficiencies at homologous and nonhomologous telomeres. Abstract Text:

Radmila Capkova Frydrychova,Harald Biessmann,Alexander Y Konev,Mikhail D Golubovsky,Jessica Johnson,Trevor K Archer,James M Mason,

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.

Transcriptional activity of the telomeric retrotransposon HeT-A in Drosophila melanogaster is stimulated as a consequence of subterminal deficiencies at homologous and nonhomologous telomeres. Publishing Authors By Initials

RC Frydrychova,H Biessmann,AY Konev,MD Golubovsky,J Johnson,TK Archer,JM Mason,

For similar genetic structures: genome: genome components: genes: transgenes research abstracts see: genetic structures: genome: genome components: genes: transgenes research

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Transcriptional activity of the telomeric retrotransposon HeT-A in Drosophila melanogaster is stimulated as a consequence of subterminal deficiencies at homologous and nonhomologous telomeres. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Intr

Journal: Molecular and cellular biology

VOLUME: 27

Page Numbers: 4991-5001

Journal Abbreviation: Mol. Cell. Biol.

ISSN: 0270-7306

DAY: 30

MONTH: 04

YEAR: 2007

Transcriptional activity of the telomeric retrotransposon HeT-A in Drosophila melanogaster is stimulated as a consequence of subterminal deficiencies at homologous and nonhomologous telomeres. Information

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LANGUAGE: eng

NlmUniqueID: 8109087

Transcriptional activity of the telomeric retrotransposon HeT-A in Drosophila melanogaster is stimulated as a consequence of subterminal deficiencies at homologous and nonhomologous telomeres. Keywords Mesh Terms:

KEYWORDS: Transgenes

MESH TERMS: genetics

Chemical & Substance for Abstract: Transcriptional activity of the telomeric retrotransposon HeT-A in Drosophila melanogaster is stimulated as a consequence of subterminal deficiencies at homologous and nonhomologous telomeres. Information

Substance Name: Retroelements

Registry Number: 0

Grant and Affiliation Information for Transcriptional activity of the telomeric retrotransposon HeT-A in Drosophila melanogaster is stimulated as a consequence of subterminal deficiencies at homologous and nonhomologous telomeres.

AFFILIATION: Laboratory of Molecular Genetics, D3-01, P.O. Box 12233, 111 T. W. Alexander Drive, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709-2233, USA.

Country: United States

AGENCY: United States NIGMS

GRANT: GM56729

ACRONYM: GM

MEDLINETA: Mol Cell Biol

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