Abstract
In wildtype males, binding of the MSL-1 gene product to the X chromosome is first seen at the cellular blastoderm stage (stage 5). MSL-2 is associated with the X chromosome in male embryos at a later stage, but the difference in apparent binding time between these two proteins is probably due to a difference in the sensitivity of their respective antisera. Early binding of MSL-1 is never seen in wildtype female embryos, and we have determined that this inhibition is mediated by the SXL product made by the activation of the early Sxl promoter. Once it is allowed to occur, the early X chromosome association of the MSLs is relatively stable, persisting in some cases through the first larval instar in spite of the presence of SXL levels concordant with normal female development. The results of these experiments are discussed in light of their relevance to the established observations that (1) the SXL made by the early promoter inhibits the hypertranscription of run at the blastoderm stage, and (2) severe disturbances in SXL function (loss in XX individuals and gain in haplo-X individuals) result in lethality during embryogenesis while loss of msl function kills males much later.
