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Dosage compensation
About: Dosage compensation is a research topic. Over the lifetime, 1920 publications have been published within this topic receiving 124589 citations.
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TL;DR: It is concluded that erosion of XCI causes a major remodelling of the proteome, with translational mechanisms affecting the expression of a much wider range of proteins and disease-linked loci than previously realised.
Abstract: Summary X chromosome inactivation (XCI) is a dosage compensation mechanism in female mammals whereby genes from one X chromosome are repressed. Analysis of human induced pluripotent stem cell (iPSC) lines using proteomics, RNAseq and polysome profiling showed a major change in the proteome upon XCI erosion. This resulted in amplified RNA and protein expression from X-linked genes. However, increased protein expression was also detected from autosomal genes without a corresponding mRNA increase, altering the protein-RNA correlation between genes on the X chromosome and autosomes. Eroded iPSC lines display ~13% increase in cell protein content, along with increased expression of ribosomal proteins, ribosome biogenesis and translation factors. They also showed significantly increased levels of active polysomes within the eroded lines. We conclude that erosion of XCI causes a major remodelling of the proteome, with translational mechanisms affecting the expression of a much wider range of proteins and disease-linked loci than previously realised.
9 citations
TL;DR: Limiting analysis and cross-specific DNA and RNA blot hybridization revealed the presence of extensive restriction pattern polymorphism and lack of sequence similarity in some areas of the 507 mr and 507 ml DNA, including the 3′ portion of the transcribed region, indicating that gene 507 is dosage compensated in D. miranda.
Abstract: The X1R chromosome of Drosophila miranda and the 3L autosome of Drosophila melanogaster are thought to have originated from the ancestral D chromosomal element and therefore may contain the same set of genes. It is expected that these genes will be dosage compensated in D. miranda because of their X linkage. To test these possibilities and to study evolution of the dosage compensation mechanism, we used the 3L-linked autosomal head-specific gene 507ml of D. melanogaster to isolate the homologous gene (507 mr) from a D. miranda genomic library. In situ hybridization showed that gene 507 is located at the 12A region of the X1R chromosome of D. miranda, indicating that the chromosomal homology deduced by cytogenetic means is correct. Restriction analysis and cross-specific DNA and RNA blot hybridization revealed the presence of extensive restriction pattern polymorphism and lack of sequence similarity in some areas of the 507 mr and 507 ml DNA, including the 3′ portion of the transcribed region. However, the 5′ portion of the transcribed region and the DNA sequences, located approximately 0.8 kb upstream and 3 kb downstream from the 507 ml gene showed a high degreee of similarity with the DNA sequences of comparable regions of the 507 mr gene. In both species gene 507 codes for a highly abundant 1.8 kb RNA which is expressed in the retina of the compound eye. Although in D. miranda the males have one and the females have two copies of the 507 gene, the steady-state levels of the 507 mRNA in both sexes were found to be similar, indicating that gene 507 is dosage compensated in D. miranda. Thus, along with the disparate rates of evolution in different areas of the DNA associated with gene 507, in D. miranda this gene has come under the regulation of the X chromosomal dosage compensation mechanism.
9 citations
TL;DR: A picture of a global landscape of sexually biased transcriptome during early B. mori embyogenesis is drawn and it is suggested for the first time that most sexually biased embryonic transcripts depend on sex chromosomes.
9 citations
01 Jan 1968
9 citations
TL;DR: A mutant Hadnl was induced in Drosophila melanogaster and found to be deficient in β-hydroxy acid dehydrogenase, and electrophoretic mobility data indicate that the enzyme is a dimer which forms by random association of subunits.
Abstract: A mutant Hadnl was induced in Drosophila melanogaster and found to be deficient in β-hydroxy acid dehydrogenase. This mutation was utilized to study the genetics and physiological expression of Had+. Had+ was mapped to the X chromosome at 54.4 and seems to be the structural gene for the enzyme. Enzyme activity in male and female flies indicates that the gene shows both dosage compensation independent from dose effect and differential activity during ontogeny. Electrophoretic mobility data indicate that the enzyme is a dimer which forms by random association of subunits. The fact that the mutant shows no detrimental effect implies that the enzyme is dispensable, at least under laboratory conditions. The biological and technical implications of this gene-enzyme system are discussed.
9 citations