Abstract
A 3.5-kb genomic DNA fragment containing the X1R chromosome-linked retina-specific Arrestin B gene (also called Arrestin 2) of Drosophila miranda (ArrB-mr) was introduced into the Drosophila melanogaster genome via germ-line transformation. The results showed that the ArrB-mr transgene was expressed only in the retina of the transformed flies. The transgene also showed male-specific transcriptional hyperactivation or dosage compensation, but the level was found to be 71-79% of the expected value. The endogenous autosomal ArrB-ml gene of D. melanogaster, as expected, was not found to be dosage compensated in the transformants. Thus, while the cis-regulatory elements for retina-specific expression are fully present in the 3.5-kb DNA, part of the sequences needed for full dosage compensation are missing in this DNA. Nucleotide (nt) sequence comparison of the upstream DNA revealed that both ArrB-mr and ArrB-ml possess a putative TATA box at -32 nt. They also have an 11-bp motif (5'-AATCCAGTTAG) similar to the photoreceptor conserved element I (PCE I) believed to play an important role in retina-specific expression of the D. melanogaster opsin and mouse Arr genes. In addition, both genes contain a TGACCT motif which is known to bind a transcription factor activated by retinoic acid and vitamin D3. However, five tandem repeats of a heptanucleotide sequence (TGGGCNR) and a 29-bp sequence with the potential to form a stem-loop structure, are found only in the ArrB-ml gene. These sequences may play an important role in dosage compensation of the X1R-linked ArrB-mr gene.
