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1.
Figure 4

Figure 4. From: Global analysis of X-chromosome dosage compensation.

Scatterplots of hybridization intensities from transformed XX;AA and X;AA tissues. Data points correspond to elements reporting autosomal genes (black) and X-chromosome genes (red). (a) XX;AA females transformed into somatic males (dsxswe/Df(3R)dsxM+15) compared with germlineless X;AA male progeny of homozygous tud1mothers and (b) XX;AA ovaries from ovo1/otu17females compared with X;AA ovaries from hs-tra83/+ males transformed into females. The expected twofold difference in gene expression in the absence of X-chromosome dosage compensation is shown as a red line.

Vaijayanti Gupta, et al. J Biol. 2006;5(1):3-3.
2.
Figure 5

Figure 5. From: Global analysis of X-chromosome dosage compensation.

Subsets of gene-expression profiles from wild-type gonads. Scatterplots of hybridization intensities for XX;AA ovary (y-axis) versus X;AA testis (x-axis) samples to elements corresponding to (a) all genes, (b) genes encoding cytoplasmic or mitochondrial proteins, and (c) de facto housekeeping genes (showing high intensity and low variance across all experiments). Data points and regression lines (trendlines) correspond to elements reporting autosomal genes (black) and X-chromosome genes (red).

Vaijayanti Gupta, et al. J Biol. 2006;5(1):3-3.
3.
Figure 10

Figure 10. From: Global analysis of X-chromosome dosage compensation.

Model for X-chromosome dosage compensation in Drosophila, C. elegans and mouse. X-chromosome transcription is generally upregulated (green arrow). X;AA tissues thus avoid unbalanced expression of X-chromosome genes. In order to avoid overexpression of X-chromosome genes (red symbols), females either destroy the compensation machinery used in males (Drosophila soma), or deploy a counteracting mechanism to reduce expression from both hyperactive X chromosomes (C. elegans) or eliminate expression from one hyperactive X chromosome (mouse). The mechanism used in the XX;AA Drosophila germline is unknown, but given that X-chromosome expression in the female germline is bi-allelic, an X-inactivation mechanism is unlikely.

Vaijayanti Gupta, et al. J Biol. 2006;5(1):3-3.
4.
Figure 8

Figure 8. From: Global analysis of X-chromosome dosage compensation.

Escaping dosage compensation. (a,b) Moving average of expression ratios plotted against position along the X chromosome (red) and autosome 2L (black) from (a) sex-transformed soma and (b) germline. (c-f) Histograms of genes showing expression ratios greater than 1.5-fold in either XX;AA (gray) or X;AA (black) transformed soma (c,d) and germline (e,f). Genotypes are indicated. Genes were analyzed by chromosome arm (number of genes >1.5-fold on arm/total on arm)/(number of genes >1.5-fold in genome/total in genome). Χ2 tests (p > 0.3) indicate that there is no enrichment on the X chromosome for genes expressed more than 1.5-fold in XX;AA soma, but that there is enrichment in gonads (*, p < 10-3).

Vaijayanti Gupta, et al. J Biol. 2006;5(1):3-3.
5.
Figure 1

Figure 1. From: Global analysis of X-chromosome dosage compensation.

Scatterplots of hybridization intensities from wild-type female and male tissues. Hybridization intensities for XX;AA vs X;AA are plotted along the y-and x-axis respectively. Data points correspond to elements reporting autosomal genes (black) and X-chromosome genes (red). (a) Germlineless XX;AA female progeny of homozygous tudor1 (tud1)) mothers (tud+ being required for germ cell formation) compared with their germlineless X;AA male siblings; (b) XX;AA wild-type ovaries compared with X;AA wild-type testes from siblings. The expected twofold difference in gene expression in the absence of X-chromosome dosage compensation is shown as a red line.

Vaijayanti Gupta, et al. J Biol. 2006;5(1):3-3.
6.
Figure 9

Figure 9. From: Global analysis of X-chromosome dosage compensation.

Scatterplots of hybridization intensities from RNA from somatic tissue from XX;AA and X;AA C. elegans and mouse. Hybridization intensities of (a) germlineless (glp4) XX;AA hermaphrodites plotted against a population greatly enriched for germlineless X;AA male C. elegans (glp4 him5), and (b) female mouse hypothalamus tissue plotted against matched tissue from males. X chromosome (red) and autosomal (black) elements as well as the trend line (red) for the twofold expression difference expected in the absence of dosage compensation are shown. (c-f) Average hybridization intensities corresponding to genes on the X chromosome (red) and autosomes (black) in (c) X;AA glp4 him5 C. elegans male soma and (d) X;AA mouse male soma (average of hypothalamus, kidney and liver) samples, (e) XX;AA glp4 C. elegans hermaphrodite soma, and (f) XX;AA mouse female soma samples. The intensities from individual autosomal arms are averaged across all experiments and standard deviations of the means are indicated.

Vaijayanti Gupta, et al. J Biol. 2006;5(1):3-3.
7.
Figure 7

Figure 7. From: Global analysis of X-chromosome dosage compensation.

Increased X-chromosome expression in the X;AA soma and germline. (a) Experimental design. The mRNA samples from XX;AA or X;AA somatic or germline tissues were labeled with either Cy3 or Cy5 and hybridized to FlyGEM arrays. Hybridization intensities corresponding to X chromosomes (red) and autosomal genes (black) were analyzed within each X:AA or XX:AA sample. (b-f) Histograms of hybridization intensities. (b) Autosomal hybridization intensities from single-copy (orange) and two-copy (black) regions of Df/+ samples in whole adult males, whole adult females and ovaries. Bars represent autosomal arms, in the order shown across the top. (c-f) Average hybridization intensities from the single X chromosome (red) compared to two copies of each autosomal arms. (c) Germlineless X;AA male progeny of homozygous tud1mothers and carcasses from X;AA males transformed into somatic females with hs-tra. (d) X;AA gonads from wildtype males and X;AA hs-tra sex transformed flies. (e) Germlineless XX;AA female progeny of homozygous tud1mothers and XX;AA females transformed into males by dsxswe/Df(3R)dsxM+15and tra2B/Df(2R)trix. (f) XX;AA gonads from wild-type and otu17/otu1and Sxl7BO/Sxlfs3transformed ovaries. Error bars show standard deviation of the mean hybridization intensity from all replicates of each sample. Numbers of hybridization replicates are indicated in parentheses above each histogram panel.

Vaijayanti Gupta, et al. J Biol. 2006;5(1):3-3.
8.
Figure 6

Figure 6. From: Global analysis of X-chromosome dosage compensation.

Gene-expression changes due to an altered gene dose on autosomes. (a) Experimental design to measure gene-expression changes for altered autosomal gene dose. Replicate mRNA samples from flies bearing a duplication, Dp(2;2)Cam3/+, or a deletion, Df(2L)JH/+, on the left arm of autosomal chromosome 2 (2L) were labeled with either Cy3 or Cy5 and hybridized to FlyGEM arrays. These were performed as dye-swap experiments to avoid any effect of dye bias. Following data extraction, changes in expression ratios as a result of differences in the dose of individual genes were determined. There are no differences in underlying gene dose outside the region of the aberrations, and there is a 1.5-fold difference when a gene is present on the duplication (Dp) or a 3-fold difference when the gene is present on the duplication and deleted in the deficiency (Df). (b) Average expression ratios from duplicate experiments comparing Dp/+ vs Df/+ adult male flies were plotted as a moving average against gene position along 2L. Gene-expression ratios for no gene dose difference (black), 1.5-fold (green) and 3-fold (orange) gene doses are indicated. Breaks in gene-expression ratios occur at the predicted cytological breakpoints of the aberrations. The aberrations are cartooned below the moving average plot, with the Dp (triangle) and Df (gap) indicated. In addition, the diploid regions of the genome where Dp/+ flies show greater expression than Df/+ flies are indicated (arrow).

Vaijayanti Gupta, et al. J Biol. 2006;5(1):3-3.
9.
Figure 3

Figure 3. From: Global analysis of X-chromosome dosage compensation.

Germline-biased gene expression in transformed ovaries. (a) Heat diagram (yellow > red > blue) of hybridization intensities for all unique array element sequences (N = 13,267) from individual samples (columns) used in this study. Gonad samples (left) and somatic samples (right) are indicated with karyotype (XX;AA and X;AA) and abbreviated genotypes; wt, wild type (see Materials and methods for more details). Replicates are indicated (brackets). Germline expression is clearly evident in the gene-expression profiles of transformed ovaries. There are large blocks of elements showing high- or low-intensity hybridization to gonad probes and the opposite pattern when hybridized to samples from carcasses or from flies lacking germ cells but having somatic components of the gonads. (b) Selected genes with known functions in the germline. Array elements representing germline-marker genes (for example, vasa (vas), pumilio (pum), tudor (tud), piwi and benign gonial cell neoplasia (bgcn) [67,68]) show strong hybridization to labeled gonad mRNA samples and comparatively weaker hybridization to non-germline samples. Furthermore, at least some of the differences between the samples also support the proposed germline sex-determination pathway. For example, as predicted, both ovo and otu are germline-biased and overexpressed in XX;AA Sxl ovaries relative to X;AA hs-tra ovaries [40,69]. All these data validate the use of XX;AA and X;AA transformed germlines as matched tissues for the careful analysis of X-chromosome dosage compensation in the germline.

Vaijayanti Gupta, et al. J Biol. 2006;5(1):3-3.
10.
Figure 2

Figure 2. From: Global analysis of X-chromosome dosage compensation.

Sex-determination hierarchy. Sex-biased expression was controlled for by using mutations in sex-determination genes. Relevant aspects of (a) wild-type female, (b) wild-type males, (c) somatic transformation from female to male (sex transformed), (d) somatic transformation from male to female (sex transformed), and (e) germline transformation are outlined. (a) Sex determination occurs in early embryogenesis, before the activation of dosage compensation, which leads to higher levels of expression of transcription factors on the X chromosome in XX;AA than X;AA individuals. These transcription factors activate Sex-lethal (Sxl) in the soma. The Sxl protein regulates the alternative splicing of the transformer (tra) pre-mRNA such that Tra protein is produced only in females. Sxl also inhibits the formation of the MSL dosage compensation complex. Tra protein and non-sex-specifically expressed Transformer2 (Tra2) protein control the alternative splicing of the doublesex (dsx) pre-mRNA. The dsx mRNAs resulting from Tra- and Tra2-mediated splicing encode a female-specific DsxF transcription factor. Sex determination in the germline is poorly understood and controversial, but a female somatic environment and an independent reading of the XX;AA karyotype in germ cells increases expression of positively acting Ovo transcription factors and their direct target, ovarian tumor (otu). The otu locus is required for Sxl activity in the germline. Note that Sxl does not regulate the MSLs in the germline. The female sex-determination hierarchy results in oogenic differentiation. (b) In X;AA flies Sxl protein is not present. This permits the formation of the MSL dosage-compensation complex. The tra pre-mRNAs are spliced to a non-coding form in the absence of Sxl, and in the absence of Tra protein the dsx pre-mRNA is spliced into a default form encoding a male-specific DsxM transcription factor. The germ cells develop into sperm. (c) XX;AA flies are transformed from females into males using null mutations of tra2 and by using a dsx mutation encoding a pre-mRNA that is constitutively spliced into the male-specific form (dsxswe). Flies bearing dsxswe in trans to a deletion produce DsxM protein and no DsxF protein. Similarly, flies null for tra2 produce only DsxM. To remove germline expression from the analysis of somatic X chromosome dosage compensation we took advantage of the fact that XX;AA flies transformed from females into males usually have no germline. These germline-atrophic (having few to no germ cells) XX;AA females transformed into males were compared with X;AA male carcasses (everything but the gonads) or with X;AA males with a genetically ablated germline due to the absence of maternal tud+. (d) X;AA flies are transformed from males into females by expressing female-specific tra cDNA transgenes. The activation of female rather than male sexual differentiation in the X;AA soma results in vast numbers of non-differentiated germ cells, presumably due to sexual incompatibility between the soma and germline. The sexual identity of these cells is ambiguous. (e) Mutations in Sxl (using allelic combinations effecting only in the germline isoforms of Sxl) or otu also result in vast numbers of non-differentiated germ cells. Positive (arrows) and negative (barred lines) genetic or molecular regulation are indicated. Loss-of-function (red) and gain-of-function (green) mutations and phenotypes are indicated.

Vaijayanti Gupta, et al. J Biol. 2006;5(1):3-3.

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