The deleterious effects of different X-chromosome dosage in males and females are buffered by a process called dosage compensation, which in Drosophila is achieved through a doubling of X-linked transcription in males. The male-specific lethal complex mediates this process, but is known to act only after gastrulation. Recent work has shown that the transcription of X-linked genes is also upregulated in males prior to gastrulation; whether it results in functional dosage compensation is not known. Absent or partial early dosage compensation raises the possibility of sex-biased expression of key developmental genes, such as the segmentation genes controlling anteroposterior patterning. We assess the functional output of early dosage compensation by measuring the expression of even-skipped (eve) with high spatiotemporal resolution in male and female embryos. We show that eve has a sexually dimorphic pattern, suggesting an interaction with either X-chromosome dose or the sex determination system. By manipulating the gene copy number of an X-linked transcription factor, giant (gt), we traced sex-biased eve patterning to gt dose, indicating that early dosage compensation is functionally incomplete. Despite sex-biased eve expression, the gene networks downstream of eve are able to produce sex-independent segmentation, a point that we establish by measuring the proportions of segments in elongated germ-band embryos. Finally, we use a whole-locus eve transgene with modified cis regulation to demonstrate that segment proportions have a sex-dependent sensitivity to subtle changes in Eve expression. The sex independence of downstream segmentation despite this sensitivity to Eve expression implies that additional autosomal gene- or pathway-specific mechanisms are required to ameliorate the effects of partial early dosage compensation.
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