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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

Published online by Cambridge University Press:  14 April 2009

A. S. Mukherjee  and
Mita Ghosh
A. S. Mukherjee
Affiliation:
Genetics Research Unit, Department of Zoology, University of Calcutta, 35 Ballygunge Circular Road, Calcutta 700 019, India
Mita Ghosh
Affiliation:
Genetics Research Unit, Department of Zoology, University of Calcutta, 35 Ballygunge Circular Road, Calcutta 700 019, India
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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 Bs. 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+(Mm). 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.

Type
Research Article
Information
Genetics Research , Volume 48 , Issue 2 , October 1986 , pp. 65 - 75
Copyright
Copyright © Cambridge University Press 1986

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