A sequence of the U5 region of Drosophila 1731 retrotransposon long terminal repeat (LTR) trans-represses the LTR-directed transcription

Transcription of retrotransposons is modulated by various upstream and down stream regulatory sites and, as in retroviruses, the majority of these site s are in long terminal repeats (LTRs). Also, various mechanisms of positive or negative regulation have been shown in the LTR of 1731, a Drosophila me lanogaster 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 exp eriments, we have been able to show that this region is implicated in tra,t s-transcriptional repression of the 1731 promoter in Schneider's Drosophila cells (S2). However, cotransfections have no effect on the UVB upregulatio n of the 1731-LTR. Also, in spite of the fact that previous experiments hav e shown that UVB irradiation activation of the 1731-LTR requires the same s hort sequence of U3 region both in drosophila cells and in a human colonic carcinoma cell line (HT29), cotransfection experiments showed that the sile ncer 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 sequenc e comparisons suggest a possible role for this putative peptide in the repr ession of transcription since this peptide has sequence similarities with s ome of the members of a family of inhibitors of transcriptional factor (Rox and Mnt proteins). Interestingly, the 1731-LTR contains the sequence CACGC G that is identical to the non-canonical E-box recognized by the Rox-Max he terodimer.