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In the present investigation the transcription and replication patterns have been examined in different segments of the X chromosome and in certain specific segments (88B-92A) of an autosomal segmental hyperploid in which an extra segment 88B-92A (3R) is translocated to the X chromosome in addition to the normal two doses. Transcriptive activity monitored by [3H]uridine-labelling of these autosomal hyperploids reveals an enhanced hyperactivity of the male X chromosome while the female X chromosomes show no change in their activity. [3H]thymidine autoradiograms reveal that while the labelling frequencies of most replicating sites are distinctly lowered in the autosomal hyperploid males, no change within sexes is resolvable with regard to labelling-intensity profile. Furthermore, the X-autosome labelling frequency relation shows a distinct deviation from linearity, suggesting multiple events that lead to a higher template form of the X chromosome. These findings lead us to suggest that the signals emanating from autosome(s) do not interfere with the primary modulation inherent in the X chromosome, but act on a modulated organization of the same at a second step evoking higher activity in the male X chromosome. The results further reveal that the gene activity of the X chromosome remains unaffected by the pattern of pairing of the autosomal segments.

Transcriptive and replicative activity of the X chromosome in an autosomal segmental hyperploid in Drosophila and its significance