Project description:Whereas in ovo exposure of genetically male (ZZ) chicken embryos to exogenous estrogens temporarily feminizes gonads at the time of hatching, the morphologically ovarian ZZ-gonads (FemZZs for feminized ZZ gonads) are masculinized back to testes within one year. To identify the feminization-resistant “memory” of genetic male sex, FemZZs showing varying degrees of feminization were subjected to transcriptomic, DNA methylome, and immunofluorescence analyses. Protein-coding genes were classified based on their relative mRNA expression across normal ZZ-testes, genetically female (ZW) ovaries, and FemZZs. We identified a group of 25 genes that were strongly expressed in both ZZ-testes and FemZZs but dramatically suppressed in ZW-ovaries. Interestingly, 84% (21/25) of these feminization-resistant testicular marker genes, including the DMRT1 master masculinizing gene, were located in chromosome Z. Expression of representative marker genes of germline cells (e.g., DAZL or DDX4/VASA) was stronger in FemZZs than normal ZZ-testes or ZW-ovaries. We also identified 231 repetitive sequences (RSs) that were strongly expressed in both ZZ-testes and FemZZs, but these RSs were not enriched in chromosome Z. Although 94% (165/176) of RSs exclusively expressed in ZW-ovaries were located in chromosome W, no feminization-inducible RS was detected in FemZZs. DNA methylome analysis distinguished FemZZs from normal ZZ- and ZW-gonads. Immunofluorescence analysis of FemZZ gonads revealed expression of DMRT1 protein in medullary SOX9+ somatic cells and apparent germline cell populations in both medulla and cortex. Taken together, our study provides evidence that both somatic and germline cell populations in morphologically feminized FemZZs maintain significant transcriptomic and epigenetic memories of genetic sex.
Project description:Gene expression was examined in genetic males that were sex-reversed to be phenotypically female compared to normal hybrid females We used microarrays to test expression in the gonad of sex-reversed females (ZZ) compared to normal females (ZW) Keywords: treatment
Project description:Gene expression was examined in genetic females that were sex-reversed to be phenotypically male compared to normal hybrid males We used microarrays to test expression in the gonad of sex-reversed males (ZW) compared to normal males (ZZ) Keywords: treatment
Project description:The contrasting dose of sex chromosomes in males and females potentially introduces a large-scale imbalance in levels of gene expression between sexes. In many organisms dosage compensation has thus evolved to equalize sex-linked gene expression in males and females1,2, in mammals achieved by X chromosome inactivation and in flies and worms by up- or down-regulation of X-linked expression, respectively. Another form of dosage compensation ensures that expression levels on the X chromosome and on autosomes are balanced3,4. While otherwise widespread in systems with heteromorphic sex chromosomes, the case of dosage compensation in birds (males ZZ, females ZW) remains an unsolved enigma5,6. Here we use a microarray approach to show that male day 18 chicken embryos generally express higher levels of Z-linked genes than female birds, both in soma and in gonads. The distribution of male-to-female fold-change values for Z chromosome genes is wide and has a mean of 1.4-1.6, which is consistent with absence of dosage compensation and sex-specific feedback regulation of gene expression at individual loci2. Intriguingly, without global dosage compensation, female chicken has significantly lower expression levels of Z-linked compared to autosomal genes, which is not the case in male birds. The pronounced sex difference in gene expression is likely to contribute to sexual dimorphism among birds, and potentially has implication to avian sex determination. Keywords: dosage compensation, sex-biased gene expression, soma and gonad
2007-08-07 | GSE8693 | GEO
Project description:ZZ/ZW sex chromosomes in the granite night lizard (Scincomorpha: Xantusiidae)
Project description:Gene expression was examined in genetic males that were sex-reversed to be phenotypically female compared to normal hybrid females; We used microarrays to test expression in the gonad of sex-reversed females (ZZ) compared to normal females (ZW) Experiment Overall Design: RNA from the ovary of sexually mature individuals was extracted and hybridized onto Affymetrix microarrays.
Project description:Gene expression was examined in genetic females that were sex-reversed to be phenotypically male compared to normal hybrid males; We used microarrays to test expression in the gonad of sex-reversed males (ZW) compared to normal males (ZZ) Experiment Overall Design: RNA from testis of sexually mature individuals was extracted and hybridized onto Affymetrix microarrays.
Project description:Birds have a sex chromosome system in which females are heterogametic (ZW) and males are homogametic (ZZ). The differentiation of avian sex chromosomes from ancestral autosomes entailed the loss of most genes from the W chromosome during evolution. However, to what extent mechanisms evolved that counterbalance the consequences of this extensive gene dosage reduction in female birds has remained unclear. Here we report functional in vivo and evolutionary analyses of a Z-chromosome-linked microRNA (miR-2954) with strongly male-biased expression that was previously proposed to play a key role in sex chromosome dosage compensation1. We knocked out miR-2954 in chicken, which resulted in early embryonic lethality of homozygous knockout males, likely due to the highly specific upregulation of dosage-sensitive Z-linked target genes of miR-2954. Our evolutionary gene expression analyses further revealed that these dosage-sensitive target genes have become upregulated on the single Z in female birds during evolution. Altogether, our work unveils a scenario where evolutionary pressures on females following W gene loss led to the evolution of transcriptional upregulation of dosage-sensitive genes on the Z not only in female but also in male birds. The resulting overabundance of transcripts in males resulting from the combined activity of two dosage-sensitive Z gene copies was in turn offset by the emergence of a highly targeted miR-2954-mediated transcript degradation mechanism during avian evolution. Our findings demonstrate that birds have evolved a unique sex chromosome dosage compensation system in which a microRNA has become essential for male survival.
Project description:Sex chromosomes evolved from autosomes many times across the eukaryote phylogeny. Several models have been proposed to explain this transition, some involving male and female sterility mutations linked in a region of suppressed recombination between X and Y (or Z/W, U/V) chromosomes. Comparative and experimental analysis of a reference genome assembly for a double haploid YY male garden asparagus (Asparagus officinalis L.) individual implicates separate but linked genes as responsible for sex determination. Dioecy has evolved recently within Asparagus and sex chromosomes are cytogenetically identical with the Y, harboring a megabase segment that is missing from the X. We show that deletion of this entire region results in a male-to-female conversion, whereas loss of a single suppressor of female development drives male-to-hermaphrodite conversion. A single copy anther-specific gene with a male sterile Arabidopsis knockout phenotype is also in the Y-specific region, supporting a two-gene model for sex chromosome evolution. Additionally, we test for the presence of Y-specific small RNA loci in several XX, XY, and YY genotypes that may be acting as sex determination loci.