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Gene expression in and development of trisomies of Drosophila melanogaster Devlin, Robert Harry


Drosophila melanoqaster individuals trisomic for an entire chromosome arm can survive to late stages of pupal development. To examine gene expression in these hyperploids, the levels of five enzymes whose structural genes are located on the left arm of chromosome two have been examined both in aneuploid and in diploid strains. Elevated levels of enzyme activity were observed in larvae possessing small segmental duplications for these genes. However, in 2L trisomies, the three distally mapping loci showed compensated levels of expression close to that observed in the diploid strains. Analysis of electrophoretic variants revealed that for one of these compensated loci all three alleles were expressed in trisomies. Two proximally located genes displayed dose-dependent levels of enzyme activity. For most genes, autosomal compensation appears to be very discrete: either the expression of the gene is repressed or it is not. To extend these observations, and to determine if autosomal compensation was peculiar to the left arm of chromosome two, trisomies for the X, for 2R, and for 3L also were examined. Compensating and non-compensating loci were also found on 3L, whereas all loci examined in X-chromosomal trisomies were dosage compensated. This suggests that X-chromosomal and autosomal trisomies are not necessarily analagous. Dosage compensation in X-chromosomal trisomies (metafemales) may occur exclusively or partially by the mechanism that operates between euploid males and females. However, some compensation in X trisomies may occur by regulatory controls distinct from male-female dosage compensation as indicated by the following results. The expression of LSP-1aT a gene that normally escapes complete dosage compensation in diploid males, was fully compensated in trisomic-X larvae. Possibly, compensation of this gene in these individuals was mediated by regulatory mechanisms other than those controlling male-female dosage compensation. As such, loci that normally do not reside on the X chromosome, but which have been transposed to this chromosome, might be expected to escape compensation in metafemales. This appears to be the case; an Adh gene that had been transposed from the second to the X chromosome was expressed at a similar level (per gene) in metafemales and females. In addition, a native X-chromosomal locus appeared to be compensated between males and females, but was not compensated in X-chromosomal trisomies. Thus, some X-linked loci escape regulation by dosage compensation in metafemales. It is possible that some of the regulatory systems operating in X-chromosomal and autosomal trisomies are analagous, and reflect a common form hyperploid compensation. The level at which compensation occured was investigated by measuring the quantities of RNA produced by several genes in whole-arm trisomies. For the heat-shock gene, hsp 85. compensation for protein levels appeared to be Post-transcriptionally regulated. However, measurements of RNA synthesis on salivary gland polytene chromosomes revealed that for most of the genes compensation was transcriptionally regulated. Dosage compensation on the autosomes probably reflects the existence of a system that normally operates in diploids to control gene expression by negative regulation.

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