A different level of X-chromosomal transcription in an In(1)BM² (reinverted) strain and in its hyperploid derivatives resolves an X-coded regulatory activity for dosage compensation in Drosophila

Abstract

The transcriptional competence of the X-chromosome of a mutant strain of Drosophila melanogaster, [in(1)BM² (reinverted)], and of hyperploid derivatives with different additional segments of the X-chromosome has been examined. The single X in the mutant male shows twice as much puffiness and RNA synthesis as does that in the normal male, revealing a level of X-coded activity in addition to the normal male and female levels. Feulgen cytophotometry reveals no duplication of DNA content in the mutant X. When duplication for the segments 1A-3E, 9A-20F, 11A-20F and 16A-20F of the X-chromosome are combined in the male with the mutant chromosome, the super-hyperactivity of the mutant X is completely abolished. In combination with the B^s. Y duplication, which contains 16A7-B2, the two-fold activity is also completely suppressed. The mutant chromosome can appear in three discrete manifestations, namely, highly flabby, intermittently flabby and normal, suggesting a leaky nature of the mutant. The effect is also temperature-sensitive. Our results suggest that there may be a modulator gene complex (M⁺) in the 16A7-B2 region as well as regulators elsewhere on the X, which in combination influence the hyperactivity of the male X in Drosophila. We suggest that the In(1)BM² (reinverted) chromosome carries a hypomorphic mutation of M⁺(M^m). The results presented here and earlier data on various X-chromosomal and autosomal hyperploids are discussed in the light of a model for dosage compensation in Drosophila.