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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
TL;DR: The mechanisms by which long non-coding RNAs function together with DNA sequence elements to tether dosage compensation complexes to the X-chromosome will be highlighted.

9 citations

Posted ContentDOI
Jiabi Chen1, Menghan Wang1, Xionglei He1, Jian-Rong Yang1, Xiaoshu Chen1 
04 Jul 2020-bioRxiv
TL;DR: Analysis showed that the fraction of dosage-sensitive housekeeping genes on the sex chromosome is significantly correlated with the S:A ratio, suggesting that the dosage sensitivity states of sex chromosomes is a major factor underlying different evolutionary strategies of dosage compensation.
Abstract: The evolution of sex chromosomes in the XY or ZW systems shall lead to gene expression dosage problems, as in at least one of the sexes, the sex-linked gene dose has been reduced by half It has been proposed, most notably by Susumu Ohno for mammals, that the transcriptional output of the whole sex chromosome should be doubled for a complete dosage compensation However, due to the variability of the existing methods to determine the transcriptional differences between Sex chromosomes and Autosomes (S:A ratios) in different studies, whether clade-specific results are comparable and whether there is a more general model to explain dosage compensation states remain unanswered In this study, we collected more than 500 public RNA-seq datasets from multiple tissues and species in major clades (including mammals, birds, fishes, insects, and worms) and proposed a unified computational framework for unbiased and comparable measurement of the S:A ratios of multiple species We also tested the evolution of dosage compensation more directly by assessing changes in the expression levels of the current sex-linked genes relative to those of the ancestral sex-linked genes We found that in mammals and birds, the S:A ratio is approximately 05, while in insects, fishes and flatworms, the S:A ratio is approximately 1 Further analysis showed that the fraction of dosage-sensitive housekeeping genes on the sex chromosome is significantly correlated with the S:A ratio In addition, the degree of degradation of the Y chromosome may be responsible for the change in the S:A ratio in mammals without a dosage-compensation mechanism Our observations offer unequivocal support for the sex chromosome insensitivity hypothesis in animals and suggest that the dosage sensitivity states of sex chromosomes is a major factor underlying different evolutionary strategies of dosage compensation

9 citations

Proceedings ArticleDOI
09 Nov 2016
TL;DR: A biocomputational platform to automatically construct large-scale mathematical models regulating the expression of several candidate genes under dosage compensation has a broader potential application to other scientific questions involving miRNA and TF networks.
Abstract: Cancer complexity and resistance is mediated by cell-to-cell heterogeneity, which is the consequence of the enormous instability of its genetic material. It is unknown how cancer cells are able to withstand the effects of these alterations, while normal cells are typically very sensitive. We hypothesize that cancer requires specific type of stability to survive the enormous chromosomal alterations. This stability may be mediated by a group of genes, whose expression is tightly regulated to maintain viability through a process called gene dosage compensation. This mechanism could be mediated by systems-level properties of complex networks of microRNAs (miRNA) and transcription factors (TF), regulating gene expression despite changes in copy number. Therefore, we designed a biocomputational platform to automatically construct large-scale mathematical models regulating the expression of several candidate genes under dosage compensation. This platform has a broader potential application to other scientific questions involving miRNA and TF networks.

9 citations

Journal ArticleDOI
TL;DR: Surprisingly, BTF3 protein levels were higher in male gonads than female gonads at embryonic day 6 (E6), suggesting translational rather than transcriptional regulation, and in gonadal sex-reversed females, RNA and protein levels of B TF3 were similar to those normally found inmale gonads, suggesting that BTF2 expression correlated with the gonadal phenotype.
Abstract: In birds, the female is heterogametic (ZW) and the male homogametic (ZZ). The small W chromosome comprises only 28 protein coding genes (homologues to Z chromosome counterparts) and a number of repeat regions. Here, we report our analysis of one of these genes, BTF3 (basic transcription factor 3), which exhibits differential expression during gonadogenesis. We measured RNA levels of both Z and W homologues and BTF3 protein levels in male and female gonads during development of the chicken embryo. In addition, BTF3 RNA and protein levels were compared in female gonads (ovary) and in female gonads following treatment to induce sex reversal (testis). Combined BTF3 RNA levels were higher in female gonads than male gonads, while BTF3-Z was expressed at similar levels in males and females. Surprisingly, BTF3 protein levels were higher in male gonads than female gonads at embryonic day 6 (E6), suggesting translational rather than transcriptional regulation. BTF3 protein was expressed in both somatic and germ cells and was restricted to the medulla of the developing ovary in females and the sex cords of the developing testis in males. In addition, in gonadal sex-reversed females, RNA and protein levels of BTF3 were similar to those normally found in male gonads, suggesting that BTF3 expression correlated with the gonadal phenotype.

8 citations

Journal ArticleDOI
TL;DR: The most likely explanation for why Lsp1 α is not dosage compensated is that the gene has not evolved a mechanism to independently recruit theMSL complex, possibly because of its recent evolutionary origin, and because there appears to be a low level of bound MSL complex in a nearby gene that is active in the same tissue.
Abstract: In Drosophila melanogaster dosage compensation of most X-linked genes is mediated by the male-specific lethal (MSL) complex, which includes MOF. MOF acetylates histone H4 at lysine 16 (H4K16ac). The X-linked Larval serum protein one α (Lsp1α) gene has long been known to be not dosage compensated. Here we have examined possible explanations for why the Lsp1α gene is not dosage compensated.

8 citations


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