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In Drosophila, the ratio of the number of X chromosomes to sets of other chromosomes initiates a series of events which result in sexual differentiation. In addition, this ratio establishes dosage compensation, a mechanism which equalizes the products of X-linked genes in males and females. The present review discusses possible genetic entities responsible for the interpretation of chromosomal sex and subsequent sex-mediated regulation during development.Key words: Drosophila, sex chromosomes, gene dosage, gene expression INTRODUCTIONIn Drosophila melanogaster, females have two X chromosomes; males have a single X and a Y. The genetic information contained by the Y chromosome i s not involved in the determination of sex. It is mostly concerned with spermatogenesis and is, therefore, necessary for male fertility. In this particular species of fruit flies, the Y chromosome also bears a cluster of ribosomal RNA cistrons. Sex is determined by the balance of X chromosomes and autosomes in the genome [ 13, and it is generally assumed that there are X-linked female-determining elements whose products are additive [2,3]. In an XX embryo, these products reach the threshold necessary to initiate sexual differentiation along a female mode. When a single X chromosome is present, the threshold is not reached and differentiation proceeds along the male mode It has long been known that, in addition to these purported sex determining genes, the X chromosome contains genes coding for basic metabolic steps or for morphological or physiological products of equal importance to males and females. With few exceptions,* the levels of these gene products are equivalent in the two sexes, leading to the notion that a mechanism exists for the compensation of gene dosage differences that normally occur between males and females.The seminal observation was reported by H.J. Muller at the Sixth International Congress of Genetics [6]. He had noted that the hypomorphic eye color mutant allele white-apricot (Mp) 276Lucchesi deficiency encompassing the gene and bearing, therefore, a single Wa allele had less pigment than homozygous females; males with an extra does of Wa had substantially darker eyes than hemizygous males. The equalization of gene products between chromosomally normal males and females led Muller to postulate the existence of a mechanism of dosage compensation for X-lined genes. He further stated that, although uncovered and more readily studied with mutants, the mechanism must operate on wild-type alleles. Validation of this point came much later with the quantitation of the activity of X-linked enzymes [7].There have been four major landmarks in the study of dosage compensation in Drosophila. The first was the evidence gathered by Mukherjee and Beerman [8] that chromosomal RNA synthesis along the single polytenic X chromosome of male larval salivary glands and the paired X chromosomes of females are equivalent, suggesting that dosage compensation is a transcriptional phenomenon. Another landmark was the demonstration that ge...
In Drosophila, the ratio of the number of X chromosomes to sets of other chromosomes initiates a series of events which result in sexual differentiation. In addition, this ratio establishes dosage compensation, a mechanism which equalizes the products of X-linked genes in males and females. The present review discusses possible genetic entities responsible for the interpretation of chromosomal sex and subsequent sex-mediated regulation during development.Key words: Drosophila, sex chromosomes, gene dosage, gene expression INTRODUCTIONIn Drosophila melanogaster, females have two X chromosomes; males have a single X and a Y. The genetic information contained by the Y chromosome i s not involved in the determination of sex. It is mostly concerned with spermatogenesis and is, therefore, necessary for male fertility. In this particular species of fruit flies, the Y chromosome also bears a cluster of ribosomal RNA cistrons. Sex is determined by the balance of X chromosomes and autosomes in the genome [ 13, and it is generally assumed that there are X-linked female-determining elements whose products are additive [2,3]. In an XX embryo, these products reach the threshold necessary to initiate sexual differentiation along a female mode. When a single X chromosome is present, the threshold is not reached and differentiation proceeds along the male mode It has long been known that, in addition to these purported sex determining genes, the X chromosome contains genes coding for basic metabolic steps or for morphological or physiological products of equal importance to males and females. With few exceptions,* the levels of these gene products are equivalent in the two sexes, leading to the notion that a mechanism exists for the compensation of gene dosage differences that normally occur between males and females.The seminal observation was reported by H.J. Muller at the Sixth International Congress of Genetics [6]. He had noted that the hypomorphic eye color mutant allele white-apricot (Mp) 276Lucchesi deficiency encompassing the gene and bearing, therefore, a single Wa allele had less pigment than homozygous females; males with an extra does of Wa had substantially darker eyes than hemizygous males. The equalization of gene products between chromosomally normal males and females led Muller to postulate the existence of a mechanism of dosage compensation for X-lined genes. He further stated that, although uncovered and more readily studied with mutants, the mechanism must operate on wild-type alleles. Validation of this point came much later with the quantitation of the activity of X-linked enzymes [7].There have been four major landmarks in the study of dosage compensation in Drosophila. The first was the evidence gathered by Mukherjee and Beerman [8] that chromosomal RNA synthesis along the single polytenic X chromosome of male larval salivary glands and the paired X chromosomes of females are equivalent, suggesting that dosage compensation is a transcriptional phenomenon. Another landmark was the demonstration that ge...
Production of trisomic-31 Drosophila melanogaster has allowed further investigation of compensated Ievels of gene expression in autosomal trisomies. We find that four enzyme loci on this arm produce diploid levels of gene product in trisomic-31 larvae. For one of these genes, we show that all three alleles are expressed at similar levels. Two genes on 3L display dose-dependent levels of gene product, and their location, relative to the four compensating loci, indicates that these two classes of genes are not regionally separated. In trisomic-2R larvae, the level of enzyme produced from on 2R-linked gene was dose dependent. In contrast, measurements of five loci on the X chromosome in metafemales (X trisomies) suggest that most genes are compensated in these individuals. Heat-shock gene expression in trisomic-31 salivary glands was qualitatively similar to diploids. The quantities of the small hsps (from the 67B cluster on 3L) suggest that these four genes respond independently to the trisomic condition; two produce compensated levels of protein, whereas the other two produce dose-dependent levels of protein. The amount of hsp 83 produced in trisomies was similar to diploids (compensated). However, quantification of hsp 83 RNA showed that a dose-dependent level of transcript was produced. This implies that hsp 83 compensation is controlled post-transcriptionally .
The classical balance concept of sex determination in Drosophila states that the X‐chromosome carries dispersed female‐determining factors. Besides, a number of autosomal genes are known that, when mutant, transform chromosomal females (XX) into pseudomales (tra), or intersexes (ix, dsx, dsxD). To test whether large duplications of the X‐chromosome have a feminizing effect on the sexual phenotype of these mutants, we constructed flies that were mutant for ix, dsx, dsxD or tra and had two X‐chromosomes plus either a distal or a proximal half of an X‐chromosome. These or even smaller X‐chromosomal fragments had a strong feminizing effect when added to triploid intersexes (XX; AAA). In the mutants, however, no shift towards femaleness was apparent. We conclude that enhancing the female determining signal is ineffective in flies that are mutant for an autosomal sex determining gene, and therefore, that these genes are under hierarchical control of the signal given by the X:A ratio. Parallels between sex‐determining and homeotic genes are drawn.
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