Differential Effects of Sex-Lethal Mutations on Dosage Compensation Early in Drosophila Development

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In response to the primary sex determination signal, X chromosome dose, the Sex-lethal gene controls all aspects of somatic sex determination and differentiation, including X chromosome dosage compensation. Two complementary classes of mutations have been identified that differentially affect Sxl somatic functions: (1) those impairing the ``early'' function used to set developmental pathway choice in response to the sex determination signal and (2) those impairing ``late'' functions involved in maintaining the pathway choice independent of the initiating signal and/or in directing differentiation. This ``early vs. late'' distinction correlates with a switch in promoter utilization from Sxl(Pe) to Sxl(Pm) at the blastoderm stage and a corresponding switch from transcriptional to RNA splicing control. Here we characterize five partial-loss-of-function Sxl alleles to explore a distinction between ``early vs. late'' functioning of Sxl in dosage compensation. Assaying for dosage compensation during the blastoderm stage, we find that the earliest phase of the dosage compensation process is controlled by products of the early Sxl promoter, Sxl(Pe). Hence, in addition to triggering the sexual pathway decision of cells, products derived from Sxl(Pe) also control early dosage compensation, the first manifestation of sexually dimorphic differentiation. The effects of mutant Sxl alleles on early dosage compensation are consistent with their previous categorization as early vs. late defective with respect to their effects on pathway initiation. Results reported here suggest that the dosage compensation regulatory genes currently known to function downstream of Sxl, genes known as the ``male-specific lethals,'' do not control all aspects of dosage compensation either at the blastoderm stage or later in development. In the course of this study, we also discovered that the canonical early defective allele, Sxl(f9), which is impaired in its ability to establish the female developmental pathway commitment, is likely to be defective in the stability and/or functioning of products derived from Sxl(Pe), rather than in the ability of Sxl(Pe) to respond to the chromosomal sex determination signal.

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