In: Biology
One of the most important decisions in development is whether to be male or female. In fruit flies most cells make this choice independent of their neighbours such that the diploid cells with one X chromosome XY are male and those with XX chromosomes are female. X-Chromosome number is relayed through regulatory proteins that act together to activate sex-lethal(sxl) in XX animals. Sxl activity is controlled by a host of transcriptional and post-tranacriptional mechanisms that tailor it's function to specific developmental scenarios. The decision of whether or not to activate sxl depends on the expression levels of four X- encoded proteins, collectively called X- linked signal elements (XSE). These four proteins encoded by the scute,sisA, runt and unpaired genes serve as the primary determinants of X dose. The XSE scute encodes a bHLH class transcription factor that , when bound to its heterodimeric partner, daughterless, directly activates sxlpe.
The pe, promoter produces RNA transcripts from which exons 2 and 3 are constituively spliced out, , resulting in an early burst of active sxl protein. Pe, however is only transiently active between embryonic cleavage cell cycles 12 and 14 and is quickly replaced by the maintenance promoter pm, which is active in both sexes and is not regulated by the numerator and denominator transcription factors. These act as transcription factors that sex specifically enhance or repress a number of downstream male and female specific genes, which implement the two different routes of sexual differentiation. Transcription factors followed a series of gene recruitment and major transtions at the top of the pathway 1) a stop codon in tra, which created a null allele, 2) the recruitment of sxl as an RNA binding factor 3) sxl autoregulation through the presence of sxl protein binding sites in sxl transcripts 4) a stop codon in sxl, which created a null allele 5) the presence of an early promoter of sxl that was activated by binding of SIS transcription factor, 6) a null allele of sis, which caused dose-dependent activation of the early promoter of sxl.