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: A model of a sexual population where deleterious mutations arise on both X and Y chromosomes is constructed and it is demonstrated that mutations on the X chromosome can considerably slow down the Muller's ratchet.
Abstract: A typical pattern in sex chromosome evolution is that Y chromosomes are small and have lost many of their genes. One mechanism that might explain the degeneration of Y chromosomes is Muller's ratchet, the perpetual stochastic loss of linkage groups carrying the fewest number of deleterious mutations. This process has been investigated theoretically mainly for asexual, haploid populations. Here, I construct a model of a sexual population where deleterious mutations arise on both X and Y chromosomes. Simulation results of this model demonstrate that mutations on the X chromosome can considerably slow down the ratchet. On the other hand, a lower mutation rate in females than in males, background selection, and the emergence of dosage compensation are expected to accelerate the process.
52 citations
TL;DR: A model in which a pre-existing active chromatin environment, coincident with H3K36me3, contributes to MSL entry site selection is supported, which can serve as a model for identifying chromatin and local sequence features that may contribute to selection of functional protein binding sites in the genome.
Abstract: The Drosophila MSL complex mediates dosage compensation by increasing transcription of the single X chromosome in males approximately two-fold. This is accomplished through recognition of the X chr ...
52 citations
TL;DR: This review highlights and discusses imprinted and random XCI from such a comparative viewpoint and indicates clear differences in the form and timing of XCI.
52 citations
TL;DR: This chapter focuses on dosage compensation in Drosophila, in which most X-linked genes are upregulated by a male-specific ribonucleoprotein complex, which is thought to recognize the X chromosome through approximately 35 dispersed chromatin entry sites and then spread in cis to dosage compensate most genes on theX chromosome.
Abstract: Just as homology can trigger a chain of events as described in many of the chapters of this volume, sometimes a lack of homology causes a crisis of a different sort. So it is for the single X chromosome in XY males in many species. Divergent sex chromosome pairs, such as the X and Y chromosomes in mammals and in fruit flies, are thought to have evolved from homologous autosomes. During evolution, the Y chromosome has retained little coding capacity, leaving the male with reduced gene dosage for many functions encoded by the X chromosome. In this chapter we focus on dosage compensation in Drosophila, in which most X-linked genes are upregulated by a male-specific ribonucleoprotein complex. This complex is thought to recognize the X chromosome through approximately 35 dispersed chromatin entry sites and then spread in cis to dosage compensate most genes on the X chromosome.
52 citations
01 Jan 1987
TL;DR: It is concluded that the most fundamental difference in X inactivation of marsupials and eutherians is whether the inactive X is the paternal one or is determined at random (with p = q in most but not all cases).
Abstract: The existence of paternal X inactivation in Australian and American marsupial species suggests that this feature of X-chromosome dosage compensation is not a recent adaptation, but probably predates the evolutionary separation of the Australian and American marsupial lineages. Although it is theoretically possible that the marsupial system is one of random X inactivation with p greater than 0.99 and q less than 0.01 and dependent on parental source, no instance of random X inactivation (p = q or p not equal to q) has ever been verified in any tissue or cell type of any marsupial species. Therefore, we conclude that the most fundamental difference in X inactivation of marsupials and eutherians is whether the inactive X is the paternal one or is determined at random (with p = q in most but not all cases). The only other unequivocal difference between eutherians and marsupials is that both X chromosomes are active in mice and human oocytes, but not in kangaroo oocytes. Apparently, the inactive X is reactivated at a later meiotic stage or during early embryogenesis in kangaroos. X-chromosome inactivation takes place early in embryogenesis of eutherians and marsupials. Extraembryonic membranes of mice exhibit paternal X inactivation, whereas those of humans seem to exhibit random X inactivation with p greater than q (i.e., preferential paternal X inactivation). In general, extraembryonic membranes of marsupial exhibit paternal X inactivation, but the Gpd locus is active on both X chromosomes in at least some cells of kangaroo yolk sac. It is difficult to draw any general conclusion because of major differences in embryogeny of mice, humans, and marsupials, and uncertainties in interpreting the data from humans. Other differences between marsupials and eutherians in patterns of X-linked gene expression and X-chromosome inactivation seem to be quantitative rather than qualitative. Partial expression of some genes on the inactive X is characteristic of marsupials, with species variation in the behavior of specific loci; some X-linked human genes on the inactive chromosome also are known to exhibit partial activity in vivo and in cultured cells. The X chromosomes of marsupials do not behave as units with respect to transcriptional activity, nor does the human X chromosome. In addition, Barr bodies have recently been detected at interphase in some marsupials, establishing that this manifestation of X chromosome inactivity is not restricted to eutherians.(ABSTRACT TRUNCATED AT 400 WORDS)
52 citations