Showing papers on "Dosage compensation published in 1977"
TL;DR: The structural gene Sgs-4 responsible for larval saliva protein 4 of Drosophila melanogaster was localized, with the help of Notch deficiencies, within the section between bands 3C10 and 3D1 of the X chromosome.
Abstract: The structural gene Sgs-4 responsible for larval saliva protein 4 of Drosophila melanogaster was localized, with the help of Notch deficiencies, within the section between bands 3C10 and 3D1 of the X chromosome. In this chromosome section there is, very probably, only one fine band. In the third larval instar chromosome this section is transcriptionally active and forms a puff. When the ecdysone concentration increases, about 5 h before prepupa formation, it becomes inactive. — In section 3C of X chromosomes of third instar larvae of the stock Hikone-R no puff is formed. The saliva of these larvae lacks protein 4. However, female hybrids (H/B and H/O) from Hikone-R crossed with Berlin and Oregon respectively produce a Hikone-specific saliva protein 4h. The synthesis of protein 4h in the hybrids H/B and H/O is ascribed to an activation of the gene Sgs-4 in the Hikone chromosome. — In the saliva of heterozygotes (FM1/H) carrying one inversion chromosome In(1) FM1 and one X chromosome from Hikone, protein 4h could not be detected. In these inversion heterozygotes in 90% of all nuclei the homologues are not paired in 3C, and 3C is puffed only in the FM1 chromosome. This suggests that a precondition for the activation of Hikone gene Sgs-4 in heterozygotes may be intimate homologue pairing. — Intersexes with one of their X chromosomes from Hikone-R and the other from Berlin produce relatively more protein 4h than do diploid H/B females, indicating facilitated transcription as a result of dosage compensation.
78 citations
TL;DR: In Drosophila melanogaster, at least five different transcriptional levels exist for X-linked structural genes; the lowest in metafemales, the highest in metamales, and three different intermediate levels, in females (diploid or triploid), intersexes and males.
Abstract: In Drosophila melanogaster , the level of X-linked gene products is found to be equivalent in normal males and females (dosage compensation) and in metafemales (3X;2A); it is also equivalent in triploid females, intersexes (2X;3A) and metamales (XY;3A). In all instances, the expression of X-linked genes is regulated in such a fashion that it is concordant with the level of autosomal gene activity. This means that at least five different transcriptional levels exist for X-linked structural genes; the lowest in metafemales, the highest in metamales, and three different intermediate levels, in females (diploid or triploid), intersexes and males. Two models have been proposed for the regulatory mechanism. These models are discussed and current experimental approaches are reviewed.
61 citations
TL;DR: The expression of another X-linked enzyme, α-galactosidase, is examined and a 300-fold increase in activity is reported, probably due to the expression of embryonic X chromosomes, during preimplantation development.
Abstract: THE most widely accepted model for X-chromosome dosage compensation in female mammals is the single-active X hypothesis (Lyon hypothesis)1. X-Chromosome dosage compensation probably occurs at about the time of implantation of the embryo into the uterus2,3 but it is not known whether this arises by a process of X-chromosome inactivation or by X-chromosome activation4. There is now good evidence for the expression of the embryonic genome during preimplantation development5–10 and Lyon2,3 has reviewed the evidence suggesting that X chromosomes are also expressed during this period. This includes both indirect observations11–13 and the more direct experiments with the X-linked enzyme hypoxanthine guanine phosphoribosyl-transferase (HPRT) (ref. 10). We have examined the expression of another X-linked enzyme, α-galactosidase14–15 and report here a 300-fold increase in activity during preimplantation development. This is probably due to the expression of embryonic X chromosomes.
50 citations
TL;DR: A single-embryo assay for HGPRT is developed of sufficient precision to establish that the distribution of activities in single embryos, half of which the authors expect to be XX and half XY, is unimodal at both the eight-cell and the blastocyst stage, concluding that dosage compensation occurs during pre-implantation development.
Abstract: THERE is strong evidence that one of the two X chromosomes is inactive in somatic cells of adult female mammals, so that the effective gene dosage per cell for X-linked loci is the same in XX females as in XY males or XO females. This system of dosage compensation is thought to be established soon after implantation1—certainly both X chromosomes seem to be potentially active in the blastocyst2. To test for dosage compensation before implantation one can study the activity of an X-chromosome-coded enzyme that is synthesised during pre-implantation development, as a result of de novo transcription, in male and female embryos. Two such enzymes are considered to be hypoxanthine phosphoribosyl transferase (HGPRT EC 2.4.2.8) and α-galactosidase3,4. Epstein3 found that groups of unfertilised eggs from XX mothers had twice the HGPRT activity found in those from XO mothers, indicating that both X chromosomes are functional during oogenesis3,5. By the morula and blastocyst stage, HGPRT activities had increased strikingly and the twofold difference had disappeared, implying that the enzyme present was no longer maternal in origin. Because pooled male and female embryos were assayed it was impossible to determine whether dosage compensation was occurring. Adler et al.4 measured α-galactosidase activity in single pre-implantation embryos, expecting that the presence of both female and male embryos would give rise to either a bimodal or a unimodal distribution of activities in the absence, or presence, respectively, of dosage compensation. The assay was insufficiently precise to give unequivocal results. We have now developed a single-embryo assay for HGPRT of sufficient precision to establish that the distribution of activities in single embryos, half of which we expect to be XX and half XY, is unimodal at both the eight-cell and the blastocyst stage. We conclude that dosage compensation occurs during pre-implantation development.
45 citations
TL;DR: In these parthenogenetic wasps, a mechanism must exist that compensates during later development for the initial two-fold difference in the chromatin content of somatic nuclei in haploid male and diploid female embryos.
Abstract: Amount of DNA-Feulgen staining in individual somatic nuclei and mature sperm of the parthenogenetic wasps, Habrobracon juglandis, H. serinopae, and Mormoniella vitripennis, were determined with a scanning microdensitometer. The haploid genome for both species of Habrobracon was estimated to be 0.15–0.16×10−12 g DNA, corresponding to a molecular weight of roughly 10×1010 daltons. The haploid genome of M. vitripennis is approximately twice this value, 0.33–0.34×10−12 g, or about 20×1010 daltons. Measurements made on dividing nuclei from syncytial preblastoderm embryos of H. juglandis and M. vitripennis showed that the chromosomes of impaternate males were present in the haploid number and contained the C amount of DNA; whereas nuclei from female preblastoderm embryos contained the diploid number of chromosomes and the 2C amount of DNA. However, hemocyte and brain cell nuclei from either male or female adult wasps contained 2C and 4C amounts of DNA. Both sexes also showed equivalent levels of polyploidy (8C, 16C, or 32C) in Malpighian tubule nuclei. Therefore, in these parthenogenetic species, a mechanism must exist that compensates during later development for the initial two-fold difference in the chromatin content of somatic nuclei in haploid male and diploid female embryos. Hemocytes from impaternate Mormoniella diploid males and triploid females contain the 2C and 3C amounts of DNA, respectively. Therefore dosage compensation involves an additional cycle of DNA replication only in haploid cells, and it insures that a certain minimum quantity of DNA is received by each somatic cell.
35 citations
TL;DR: The XO sex chromosome constitution has been found in both sexes of the mole-vole and the presence in XO males and the absence from XO females of H-Y (histocompatibility Y) antigen is revealed, indicating the testis-organizing function of the H-y gene appears to have been confirmed.
26 citations
TL;DR: Measurements are presented as experimental evidence that, in Drosophila melanogaster, an autosomal gene relocated to the X chromosome is not dosage compensated, andldehyde oxidase activity has been measured.
Abstract: Aldehyde oxidase activity has been measured in flies with the structural gene for this enzyme translocated to the X chromosome. These measurements are presented as experimental evidence that, in Drosophila melanogaster, an autosomal gene relocated to the X chromosome is not dosage compensated.
17 citations
TL;DR: In this paper, the authors examined thymidine labeling patterns in gynandric mosaic salivary glands of drosophila melanogaster and found that the X chromosome of the XO2A cells always had fewer sites labeled than the X chromosomes of the XX2A nuclei, for a given pattern of the autosomes in either sex.
Abstract: [(3)H]Thymidine labeling patterns have been examined in gynandric mosaic salivary glands of drosophila melanogaster. The Ring-X stock, R(1) w(ve)/In(1)dl 49, l (1) J1 y w lz(s), was used for this purpose. 365 labeled XX2A and 40 labeled XO2A nuclei were obtained from a total of 624 nuclei in nine pairs of mosaic salivary glands. It was observed that in all but those nuclei which had DD, 1C, and 2C patterns, the X chromosome of the XO2A nuclei always had fewer sites labeled than the X chromosomes of the XX2A nuclei, for a given pattern of the autosomes in either sex. Such asynchronous labeling of the X chromosome in the XO2A (male) nuclei was observed regardless of the proportion of the XO2A cells (2.0-73.7 percent), in the mosaic glands. Moreover, while the frequency of [(3)H]thymidine labeling for all of the 39 replicating units except the two late replicating sites (3C and 11A) in the X chromosome of the XO2A nuclei, was consistently lower than in the X chromosome of the XX2A nuclei, the mean number of grains on the X chromosome was relatively (to autosomes) similar in both XX2A and XO2A cells. The results, therefore, suggest that, as in XY2A larval glands, the X chromosome in the XO2A cells also completes the replication earlier than autosomes and that the XO2A nuclei show cellular autonomy with respect to the early replication of the X chromosome, like its counterpart, RNA transcription. Absence of the asynchrony during the initial phase (DD-2C) further completes the replication earlier but that the rate of replication of its DNA is possibly faster, and (b) that there might be a common regulation with respect to the initiation of replication of different chromosomes in a genome.
15 citations
TL;DR: Results indicate that dosage compensation is complete (or nearly so) for sex-linked genes affecting this character, and dosage compensation does not operate by paternal X inactivation.
Abstract: Seventeen lines, each homozygous for a different X chromosome but all with a common autosomal genetic blackground, were constructed and assayed for abdominal bristle number to determine whether dosage compensation operates for sex-linked genes affecting this character. --The regression coefficient of male mean on female mean using a logarithmic scale was 0.90 +/- 0.13 and the genetic regression coefficient 0.92, neither differing significantly from unity. The genetic components of variance in males and females were also very similar (0.000234 or 0.000228, respectively). These results indicate that dosage compensation is complete (or nearly so) for sex-linked genes affecting this character. The bristle scores of females did not differ in reciprocal crosses between these lines, thus dosage compensation does not operate by paternal X inactivation. --The question of an adequate scale for abdominal bristle number had to be examined during the study. A logarithmic scale appeared to be adequate for both genotypic and environmental differences.
10 citations
TL;DR: Various arguments and some experimental evidence discounting controlled variation of total template as the basis for dosage compensation in Drosophila melanogaster are presented.
Abstract: DOSAGE compensation is the equalisation of X-linked gene products in males and females. In Drosophila there is substantial evidence to support the contention that both X chromosomes are simultaneously active in somatic cells of females1, and that the regulatory mechanism operates at the level of transcription2,3. Most discussions of this mechanism have focused on the modulation of regulatory factors controlling the rate of RNA synthesis per template4,5. A change in the level of transcription may also be achieved by altering the quantity of template. We present here various arguments and some experimental evidence discounting controlled variation of total template as the basis for dosage compensation in Drosophila melanogaster.
6 citations