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Transcription in X-chromosomal segmental aneuploids of Drosophila melanogaster and regulation of dosage compensation

Published online by Cambridge University Press:  14 April 2009

Jayashree Prasad ,
Ashish K. Duttagupta  and
A. S. Mukherjee
Jayashree Prasad
Affiliation:
Genetics Research Unit, Department of Zoology, University of Calcutta, 35 Ballygunge Circular Road, Calcutta 700 019, India
Ashish K. Duttagupta
Affiliation:
Genetics Research Unit, Department of Zoology, University of Calcutta, 35 Ballygunge Circular Road, Calcutta 700 019, India
A. S. Mukherjee
Affiliation:
Genetics Research Unit, Department of Zoology, University of Calcutta, 35 Ballygunge Circular Road, Calcutta 700 019, India

Summary

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Transcription of X chromosomal DNA has been examined autoradio-graphically in various 1X2A and 2X2A normal larvae and 1X2A (+ X fr) and 2X2A (+ X fr) segmental aneuploid larvae of species Drosophila melanogaster. The segmental aneuploids contained duplications for the segment 9A–11A and 15D–ISA of the X chromosome. Results show that in the aneuploid male containing 9A–11A duplicaton both the homologous segments involved in the aneuploidy are autonomously hyperactive; their combined activity, measured by X/A grain ratio, is found to be nearly 70% more than the activity in normal male and about 100% more than that in diplo-X female. In the aneuploid female, containing the aneuploid segment 15D–18A and having three doses of the segment of the X chromosome, the activity was over 100% more than the diplo-X activity. The per gene dose activity for the two segments in the aneuploid male and female, respectively, is also significantly higher than their male and female counterparts. The possible role of lack of contiguity of the genetic segments and an intra-nuclear variation has been ruled out by appropriate analysis. We, therefore, interpret these findings to be due to an autonomous expression of the X linked compensatory genes, resulting from a primary modulation in the organization of the entire X chromosome. The autosomal signal then renders the individual genetic locus hyperactive.

Type
Research Article
Information
Genetics Research , Volume 38 , Issue 2 , October 1981 , pp. 103 - 113
Copyright
Copyright © Cambridge University Press 1981

References

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