Topic
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 demonstrated that male X chromosome genes that are located in repressive chromatin states are depleted of MSL occupancy; however, they show dosage compensation, suggesting this non-canonical dosage compensation is due to the same transacting derepression that occurs on autosomes.
Abstract: In animals with XY sex chromosomes, X-linked genes from a single X chromosome in males are imbalanced relative to autosomal genes. To minimize the impact of genic imbalance in male Drosophila, there is a dosage compensation complex (MSL) that equilibrates X-linked gene expression with the autosomes. There are other potential contributions to dosage compensation. Hemizygous autosomal genes located in repressive chromatin domains are often derepressed. If this homolog-dependent repression occurs on the X, which has no pairing partner, then derepression could contribute to male dosage compensation. We asked whether different chromatin states or topological associations correlate with X chromosome dosage compensation, especially in regions with little MSL occupancy. Our analyses demonstrated that male X chromosome genes that are located in repressive chromatin states are depleted of MSL occupancy; however, they show dosage compensation. The genes in these repressive regions were also less sensitive to knockdown of MSL components. Our results suggest that this non-canonical dosage compensation is due to the same transacting derepression that occurs on autosomes. This mechanism would facilitate immediate compensation during the evolution of sex chromosomes from autosomes. This mechanism is similar to that of C. elegans, where enhanced recruitment of X chromosomes to the nuclear lamina dampens X chromosome expression as part of the dosage compensation response in XX individuals.
7 citations
TL;DR: It is shown that loss of Pof decreases not only chromosome 4 expression but also reduces the X-chromosome expression in males, and the role of the 1.688 satellite in hybrid lethality is discussed.
Abstract: Chromosome-specific regulatory mechanisms provide a model to understand the coordinated regulation of genes on entire chromosomes or on larger genomic regions. In fruit flies, two chromosome-wide systems have been characterized: The male-specific lethal (MSL) complex, which mediates dosage compensation and primarily acts on the male X-chromosome, and Painting of fourth (POF), which governs chromosome-specific regulation of genes located on the 4th chromosome. How targeting of one specific chromosome evolves is still not understood; but repeated sequences, in forms of satellites and transposable elements, are thought to facilitate the evolution of chromosome-specific targeting. The highly repetitive 1.688 satellite has been functionally connected to both these systems. Considering the rapid evolution and the necessarily constant adaptation of regulatory mechanisms, such as dosage compensation, we hypothesised that POF and/or 1.688 may still show traces of dosage-compensation functions. Here, we test this hypothesis by transcriptome analysis. We show that loss of Pof decreases not only chromosome 4 expression but also reduces the X-chromosome expression in males. The 1.688 repeat deletion, Zhr1 (Zygotic hybrid rescue), does not affect male dosage compensation detectably; however, Zhr1 in females causes a stimulatory effect on X-linked genes with a strong binding affinity to the MSL complex (genes close to high-affinity sites). Lack of pericentromeric 1.688 also affected 1.688 expression in trans and was linked to the differential expression of genes involved in eggshell formation. We discuss our results with reference to the connections between POF, the 1.688 satellite and dosage compensation, and the role of the 1.688 satellite in hybrid lethality.
7 citations
TL;DR: In this article, a nuclear pore component, called Mtor, is shown to be involved in setting the correct levels of transcription from the male X chromosome in Drosophila melanogaster.
7 citations
TL;DR: In this paper, the authors show that male-heterogamy alone is not sufficient to explain the reduced efficacy of selection on the bird Z chromosome, and instead, a combination of patterns of dosage compensation and overall effective population size, among other factors, influence patterns of faster-Z evolution.
Abstract: Genes linked to X or Z chromosomes, which are hemizygous in the heterogametic sex, are predicted to evolve at different rates than those on autosomes. This faster-X effect can arise either as a consequence of hemizygosity, which leads to more efficient selection for recessive beneficial mutations in the heterogametic sex, or as a consequence of reduced effective population size of the hemizygous chromosome, which leads to increased fixation of weakly deleterious mutations due to random genetic drift. Empirical results to date have suggested that, while the overall pattern across taxa is complicated, in general systems with male-heterogamy show a faster-X effect primarily attributable to more efficient selection while the only female-heterogamy taxon studied to date (birds) shows a faster-Z effect primarily attributable to increased drift. In order to test the generality of the faster-Z pattern seen in birds, we sequenced the genome of the Lepidopteran insect Bombyx huttoni, a close outgroup of the domesticated silkmoth Bombyx mori. We show that silkmoths experience faster-Z evolution, but unlike in birds, the faster-Z effect appears to be attributable to more efficient positive selection in females. These results suggest that female-heterogamy alone is unlikely to be sufficient to explain the reduced efficacy of selection on the bird Z chromosome. Instead, it is likely that a combination of patterns of dosage compensation and overall effective population size, among other factors, influence patterns of faster-Z evolution.
7 citations
TL;DR: Evidence is provided which supports the possibility that dosage compensation in X-chromosomal trisomies (metafemales) can occur by a mechanism distinct from the regulatory system that operates to equalize gene expression between euploid males and females.
Abstract: In this study, we provide evidence which supports the possibility that dosage compensation in X-chromosomal trisomies (metafemales) can occur by a mechanism distinct from the regulatory system that operates to equalize gene expression between euploid males and females. This hypothesis is based on the strong parallelism between compensation in X and autosomal trisomies, and is supported by two sets of observations. First, two genes that are compensated between males and females are not compensated in metafemales. These include the gene Adh which was inserted into the X by transformation, and the malic enzyme regulatory gene whose natural site of residence is the X chromosome. Second, a gene that escapes compensation in euploid males and females (LSP-1α), is fully compensated in X-chromosomal trisomies. Measurements of RNA and protein products of this gene suggest that compensation in metafemales occurs at the level of transcription.
7 citations