Abstract

A Sequence of the U5 Region of Drosophila 1731 Retrotransposon Long Terminal Repeat (LTR) Trans-represses the LTR-directed Transcription

E. Faure

Case 31, ICB, UPRES 2202 Biodiversité, Université de Provence, 13331 Marseille, cedex 3, France; fax: 33 491 10 63 53; E-mail: e_faure@hotmail.com

Received August 3, 1998; Revision received December 7, 1998
Transcription of retrotransposons is modulated by various upstream and downstream regulatory sites and, as in retroviruses, the majority of these sites are in long terminal repeats (LTRs). Also, various mechanisms of positive or negative regulation have been shown in the LTR of 1731, a Drosophila melanogaster retrotransposon. Here we describe experiments investigating the possible mechanism of action of a region localized in the U5 region of the 1731-LTR, which has been considered as a silencer. Using cotransfection experiments, we have been able to show that this region is implicated in trans-transcriptional repression of the 1731 promoter in Schneider's Drosophila cells (S2). However, cotransfections have no effect on the UV-B upregulation of the 1731-LTR. Also, in spite of the fact that previous experiments have shown that UV-B irradiation activation of the 1731-LTR requires the same short sequence of U3 region both in drosophila cells and in a human colonic carcinoma cell line (HT29), cotransfection experiments showed that the silencer of the U5 region has no significant effect in human cells. Analysis of the U5 region shows the presence of a short open reading frame which could encode a 26 amino acid polypeptide. Furthermore, computer assisted sequence comparisons suggest a possible role for this putative peptide in the repression of transcription since this peptide has sequence similarities with some of the members of a family of inhibitors of transcriptional factor (Rox and Mnt proteins). Interestingly, the 1731-LTR contains the sequence CACGCG that is identical to the non-canonical E-box recognized by the Rox--Max heterodimer.
KEY WORDS: 1731, coevolution, Drosophila melanogaster, HIV-1, LTR, negative regulation, retrotransposon, UV irradiation