DOSAGE COMPENSATION FOR ENZYME ACTIVITIES IN
            <i>Drosophila melanogaster</i>

Seecof, Robert L.; Kaplan, William D.; Futch, David G.

doi:10.1073/pnas.62.2.528

Cited by 67 publications

(19 citation statements)

References 7 publications

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“…For a variety of organisms, duplication or deletion of a segment of the genome containing a given structural gene are known to elevate or depress the levels of the latter's protein product (Grell, 1962(Grell, , 1969Ciferri, Sora & Tiboni, 1969;Seecof, Kaplan & Futch, 1969;Nielson & Frydenberg, 1971). By analogy with these structural gene systems, the intracellular concentration of the product of a regulatory gene is probably related to the number of copies of the gene present in the cell.…”

Section: Introductionmentioning

confidence: 99%

Regulation of enzyme activities inDrosophila: I. The detection of regulatory loci by gene dosage responses

Rawls

Lucchesi

1974

Genet. Res.

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In order to detect regulatory genetic sites in the autosomes of Drosophila melanogaster, the levels of X-linked glucose-6-phosphate dehydrogenase and autosomally linked a-glycerophosphate and isocitrate dehydrogenases have been monitored in extracts of flies aneuploid for regions of chromosomes II and III. In addition to expected structural gene dosage responses of a-GPDH and IDH, flies hyperploid for several autosome regions were found to display altered levels of one or more of the enzymes studied. While IDH activity was increased in flies hyperploid for segments of both chromosomes II and III, a-GPDH activity was decreased in specific hyperploids for chromosome II regions only. The latter group of segmental aneuploids were normal with respect to levels of chromosome II-linked alcohol dehydrogenase. To test if the observed responses were due to dosage changes of discrete genes lying within the larger effective segments, flies aneuploid for subdivisions of the chromosome segments 21A-25CD, 35A-40, and 70CD-71B were assayed. For two of these large segments so analysed, the apparent effects were attributable to specific small subdivisions, suggesting the presence of discrete regulatory sites within the latter. For the 35A-40 region the a-GPDH effect observed for subdivisions was not sufficient to account for the large a-GPDH decrease seen in flies hyperploid for the large, inclusive region. These observations are discussed with respect to the possible bases of effect of regulatory elements on enzyme activity.

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Section: Introductionmentioning

confidence: 99%

Regulation of enzyme activities inDrosophila: I. The detection of regulatory loci by gene dosage responses

Rawls

Lucchesi

1974

Genet. Res.

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“…The mechanism occurs at the level of transcription (2) and is dependent upon the activity of one or more autosomal genes (3)(4)(5)(6). Xlinked genes need not be located on the X chromosome to be dosage-compensated, since (a) X chromosome genes translocated to autosomes still exhibit compensation (7)(8)(9)(10)(11) and (b) autosomal regions inserted into the X do not exhibit compensation (12,13). Therefore, the regulatory elements responsible for dosage compensation are probably interspersed along the X chromosomes.…”

mentioning

confidence: 99%

Incomplete dosage compensation in an evolving Drosophila sex chromosome.

Strobel¹,

Pelling²,

Arnheim³

1978

Proc. Natl. Acad. Sci. U.S.A.

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Cellular autoradiography was used to measure relative rates of chromosomal RNA synthesis and to examine the regulatory phenomenon of X-linked dosage compensation in Drosophila Miranda, a species containing two distinct, nonhomologous X chromosomes (X' and X2). The XI chromosome was found to be dosage-compensated, since the rate of RNA synthesis along the single XI chromosome in males equaled that of both XI chromosomes in females. Unlike other sex chromosomes that have been studied, the more recently evolved X2 heterochromosome exhibited regional differences in transcriptional activity when males and females were compared. The distal 10% of the X2 was not dosage-compensated, whereas the majority of an interior segment, representing 30% of the X2 chromosome's length, was found to be dosage-compensated. Our data are consistent with the idea that the evolution of X2 dosage compensation has paralleled the differentiation of the X2 sex chromosome. In addition, gene rearrangement seems to have accompanied the acquisition of a dosage-compensatory mechanism in the X2. The phenomenon of dosage compensation in Drosophila has been examined in a number of species within the genus. In all cases it appears as if a regulatory system modulates the amount of X chromosome gene products formed in such a way that males with one X chromosome and females with two X chromosomes have equal amounts of product. An X-linked gene is therefore twice as active in males as in females (1). The mechanism occurs at the level of transcription (2) and is dependent upon the activity of one or more autosomal genes (3-6). Xlinked genes need not be located on the X chromosome to be dosage-compensated, since (a) X chromosome genes translocated to autosomes still exhibit compensation (7-11) and (b) autosomal regions inserted into the X do not exhibit compensation (12, 13). Therefore, the regulatory elements responsible for dosage compensation are probably interspersed along the X chromosomes.As an approach toward understanding the evolution of dosage-compensatory mechanisms, we have examined a Drosophila species that has recently undergone evolutionary differentiation of its sex chromosomes. Drosophila miranda, which exhibits a unique sex-chromosome constitution, is a morphologically similar, reproductively compatible sibling species of D. pseudoobscura (14). D. miranda has two chromosomes (X' and X2), each of which exists in a single copy in males and in two copies in females (15). Both arms of the XI chromosome are homologous to the X chromosome arms of D. pseudoobscura, whereas the X2 is largely homologous to the autosomal third chromosome of D. pseudoobscura (15). The X2 evolved as a consequence of a Y-3 chromosomal fusion in the D. miranda lineage (16). Ancestral males are presumed to have had one copy of the new Y-3 fusion chromosome and one copy of the "free" third chromosome, whereas females had two copies of the latter. Eventually, most third chromosome genes on the new Y degenerated, and the "free" third chromosome gradually differenti...

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“…6, the size of the G6PD mRNA in adult male and female flies is 2.0 kb, and the steady-state levels of the mRNAs in the somatic cells of the two sexes are similar. This observation indicates that similar levels of G6PD enzyme activity in the two sexes (Seecof et al, 1969) is due to the steady-state level of G6PD mRNA. Also, it supports the previous conclusions, based on studies using salivary gland chromosomes (Mukherjee and Beermann, 1965), that dosage compensation is the result of increased transcriptional activity of the male X chromosome.…”

Section: (B) Wpd Mrnamentioning

confidence: 69%