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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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Journal ArticleDOI
01 Nov 2002-Genesis
TL;DR: Analysis of interactions with mutations in the major sex‐determining genes show that sup‐26 and sup‐27 influence sex determination in fundamentally different ways.
Abstract: Summary: The her-1 regulatory switch gene in C. elegans sex determination is normally active in XO animals, resulting in male development, and inactive in XX animals, allowing hermaphrodite development. The her-1(n695gf) mutation results in the incomplete transformation of XX animals into phenotypic males. We describe four extragenic mutations that suppress the masculinized phenotype of her-1(n695gf) XX. They define two previously undescribed genes, sup-26 and sup-27. All four mutations exhibit semidominance of suppression and by themselves have no visible effects on sex determination in otherwise genotypically wild-type XX or XO animals. Analysis of interactions with mutations in the major sex-determining genes show that sup-26 and sup-27 influence sex determination in fundamentally different ways. sup-26 appears to act independently of her-1 to negatively modulate synthesis or function of tra-2 in both XX and XO animals. sup-27 may play a role in X-chromosome dosage compensation and influence sex determination indirectly. genesis 34:184–195, 2002. © 2002 Wiley-Liss, Inc.

8 citations

Journal ArticleDOI
TL;DR: The dosage compensation complex (DCC) of Drosophila identifies its X-chromosomal binding sites with exquisite selectivity as mentioned in this paper, and the principles that assure this vital targeting are known from the D. melanogaster model: DCC-intrinsic specificity of DNA binding, cooperativity with the CLAMP protein, and noncoding roX2 RNA transcribed from the X chromosome.
Abstract: The dosage compensation complex (DCC) of Drosophila identifies its X-chromosomal binding sites with exquisite selectivity. The principles that assure this vital targeting are known from the D. melanogaster model: DCC-intrinsic specificity of DNA binding, cooperativity with the CLAMP protein, and noncoding roX2 RNA transcribed from the X chromosome. We found that in D. virilis, a species separated from melanogaster by 40 million years of evolution, all principles are active but contribute differently to X specificity. In melanogaster, the DCC subunit MSL2 evolved intrinsic DNA-binding selectivity for rare PionX sites, which mark the X chromosome. In virilis, PionX motifs are abundant and not X-enriched. Accordingly, MSL2 lacks specific recognition. Here, roX2 RNA plays a more instructive role, counteracting a nonproductive interaction of CLAMP and modulating DCC binding selectivity. Remarkably, roX2 triggers a stable chromatin binding mode characteristic of DCC. Evidently, X-specific regulation is achieved by divergent evolution of protein, DNA, and RNA components.

8 citations

Journal ArticleDOI
TL;DR: A three-step model of DC evolution is proposed: once recombination ceases and the Y begins to deteriorate, genes from longer metabolic pathways should be lost first, as halving these genes does not drastically reduce flux or fitness, thereby, fitness.
Abstract: We explore the evolutionary origins of dosage compensation (DC) in sex chromosomes in the context of metabolic control theory. We consider first the cost of gene loss (hemizygosity) per se in reducing flux, and examine two relationships between flux and fitness (linear and Gaussian) to calculate a fitness cost of hemizygosity. Recognizing that new sex chromosomes are derived from autosomes, we also calculate the cost of unmasking deleterious mutations segregating on the nascent sex chromosomes as loci become hemizygous. The importance of deleterious mutations to the fitness cost of hemizygosity depends on their frequency, and on the relative costs of halving gene dose for wild-type alleles. We then consider the evolution of DC in response to gene loss, and include a cost of overexpression (i.e., DC such that expression exceeds the wild-type homozygote). Even with costs to excess flux, hypomorphic mutations can cause the optimal level of DC to be higher than 2-fold when the absolute cost of hemizygosity is small. Finally, we propose a three-step model of DC evolution: 1) once recombination ceases and the Y begins to deteriorate, genes from longer metabolic pathways should be lost first, as halving these genes does not drastically reduce flux or, thereby, fitness; 2) both the cost of hemizygosity and the presence of hypomorphic mutations will drive an increase in expression, that is, DC; 3) existing DC will now permit loss of genes in short pathways.

8 citations

Journal ArticleDOI
TL;DR: The results show that the MAO-A gene has mono-allelic expression in primary clonal cell cultures, which could have important implications for understanding traits that display gender differences.
Abstract: X chromosome inactivation in mammalian females occurs early in embryonic development and renders most genes on the inactive X chromosome transcriptionally silenced. As a consequence, females will display an X chromosomal parent-of-origin mosaicism with regard to which parental allele that is expressed. Some genes however, escape inactivation and will therefore be expressed from both alleles. In this study we have investigated if the X-linked MAO-A gene have bi- or mono-allelic expression. This information would indicate whether or not MAO-A gene dosage could potentially explain the observed gender differences that show functional connections to the serotonin system, such as aggression and impulsiveness. To investigate the X inactivation status of MAO-A we have used primary clonal cell cultures, on which allelic expression was assessed with RFLP analysis. Our results show that the MAO-A gene has mono-allelic expression in these cells. This could have important implications for understanding traits that display gender differences.

8 citations

Journal ArticleDOI
TL;DR: This is the first next-generation sequencing report showing DC in B. mori, clarifying the previous contradictions and suggesting a complete but an unconventional type of DC, which may be achieved by reduced Z-linked expression in males (ZZ).
Abstract: Sex chromosomal dose difference between sexes is often normalized by a gene regulatory mechanism called dosage compensation (DC). Studies indicate that DC mechanisms are generally effective in XY r...

8 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202330
202272
202183
202051
201980
201870