Abstract
mRNAs from the early Sex-lethal promoter, Sxl-Pe, encode embryonic Sxl proteins that function to activate the Sxl autoregulatory loop. They do so by directing the female-specific splicing of the first transcripts expressed from the late or maintenance promoter, Sxl-Pm. The early promoter is located, however, upstream not downstream of the translation terminating male-specific exon, L3, and upstream of the second Sxl-Pm exon, L2. If the Sxl proteins expressed from Sxl-Pe are to provide the mechanism for bypassing the normal requirement for Sxl protein in the female-specific splicing of transcripts from Sxl-Pm, then what is the mechanism for skipping L2 and L3 in the processing of transcripts from Sxl-Pe? In the studies reported here, we have generated a report construct to examine the splicing of Sxl-Pe transcripts. Our results indicate that neither specific maternal products, Sxl protein, nor an X chromosome to autosome ratio of 1 are required for the processing of the embryonic mRNAs. We also found that none of the three genes, snf, virilizer, and fl(2)d, which when mutated alter the female-specific processing of Sxl-Pm transcripts, alter the generation of the early splice. Skipping to intervening exons to generate an open reading frame that will encode the Sxl early proteins appears to be an intrinsic property of initiating the early Sxl RNAs within the first intron of the Sxl-Pm maintenance transcription unit.
