Topic
Dosage compensation
About: Dosage compensation is a research topic. Over the lifetime, 1920 publications have been published within this topic receiving 124589 citations.
Papers published on a yearly basis
Papers
More filters
TL;DR: The evolution of dosage compensation and how it is controlled during embryogenesis of mammals is discussed and the potential role of X chromosome number during early development is summarized.
75 citations
TL;DR: It is demonstrated that SXL inhibits translation initiation and prevents the stable association of the 40S ribosomal subunit with the mRNA in a manner that does not require the presence of a cap structure at the 5' end of the mRNA.
75 citations
TL;DR: This work has used a modification of Kanda's method, which renders the presumptive inactive X dark staining, to reveal an inactive X chromosome in both endoderm and mesoderm layers of separated yolk sacs from parthenogenones, indicating that even in tissues in which there is normally total non-random paternal X inactivation, a maternally derived X can be inactivated.
Abstract: In somatic cells of female mammals one of the two X chromosomes is genetically inactive and heterochromatic, resulting in dosage compensation for X-linked genes1–3. In marsupials the paternally derived X chromosome is preferentially inactivated. In eutherian mammals, although either X chromosome can be inactivated at random in somatic cells, preferential inactivation of the paternally derived X chromosome has been demonstrated cytologically in mouse and rat yolk sac5,6 and mouse chorion5 and biochemically in mouse yolk sac7, chorionic ectoderm8 and trophoblast. In mouse yolk sac the non-random element has been shown both biochemically7 and cytologically9 to be confined to the endoderm layer in which there is almost total paternal X-chromosome inactivation. We have therefore looked at X-chromosome activity in the separated yolk sac layers of diploid parthenogenetic mouse embryos in which both X chromosomes are maternally derived. Kaufman et al.10 have demonstrated X inactivation in somatic cells of diploid parthenogenetic embryos, and we have used a modification of Kanda's method11, which renders the presumptive inactive X dark staining, to reveal an inactive X chromosome in both endoderm and mesoderm layers of separated yolk sacs from parthenogenones. Thus even in tissues in which there is normally total non-random paternal X inactivation, in the absence of a paternally derived X chromosome a maternally derived X can be inactivated.
75 citations
TL;DR: A region of H4 hyperacetylation extending up to 120 kb upstream from the Xist somatic promoter P1 is identified, which includes the promoter P0, which gives rise to the unstable Xist transcript in undifferentiated cells.
Abstract: We have investigated the role of histone acetylation in X chromosome inactivation, focusing on its possible involvement in the regulation of Xist, an essential gene expressed only from the inactive X (Xi). We have identified a region of H4 hyperacetylation extending up to 120 kb upstream from the Xist somatic promoter P1. This domain includes the promoter P0, which gives rise to the unstable Xist transcript in undifferentiated cells. The hyperacetylated domain was not seen in male cells or in female XT67E1 cells, a mutant cell line heterozygous for a partially deleted Xist allele and in which an increased number of cells fail to undergo X inactivation. The hyperacetylation upstream of Xist was lost by day 7 of differentiation, when X inactivation was essentially complete. Wild-type cells differentiated in the presence of the histone deacetylase inhibitor Trichostatin A were prevented from forming a normally inactivated X, as judged by the frequency of underacetylated X chromosomes detected by immunofluorescence microscopy. Mutant XT67E1 cells, lacking hyperacetylation upstream of Xist, were less affected. We propose that (i) hyperacetylation of chromatin upstream of Xist facilitates the promoter switch that leads to stabilization of the Xist transcript and (ii) that the subsequent deacetylation of this region is essential for the further progression of X inactivation.
75 citations
TL;DR: This work explores recent advances in the study of vertebrate sex chromosomes achieved using genomic analyses using whole genome sequences from a variety of organisms.
Abstract: Sex chromosomes have evolved multiple times in many taxa. The recent explosion in the availability of whole genome sequences from a variety of organisms makes it possible to investigate sex chromosome evolution within and across genomes. Comparative genomic studies have shown that quite distant species may share fundamental properties of sex chromosome evolution, while very similar species can evolve unique sex chromosome systems. Furthermore, within-species genomic analyses can illuminate chromosome-wide sequence and expression polymorphisms. Here, we explore recent advances in the study of vertebrate sex chromosomes achieved using genomic analyses.
75 citations