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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: Spreading of dosage compensation over the X chromosome in Drosophila males requires the noncoding roX1 and roX2 RNAs, which contain discrete binding sites that are remodeled during assembly of the dosage compensation complex.

6 citations

Journal ArticleDOI
01 Aug 1991
TL;DR: It is concluded that the gene fl(2)d seems to be necessary during the adult life of females for the processes that require Sxl+ activity, and the SxL-independent vital function of fl( 2)d appears to be required in both sexes only during larval development.
Abstract: In Drosophila melanogaster, the gene Sex-lethal (Sxl) controls the processes of sex determination, dosage compensation, oogenesis and sexual behaviour. The control of Sxl is by alternative splicing of its primary RNA. We have identified a gene, female-lethal-2-d (fl(2)d), which is needed for the female-specific splicing of Sxl RNA and which also has a vital function independent of Sxl. Here we analyse other aspects of the gene fl(2)d. Specifically, we have analysed the effect of the temperature-sensitive mutation fl(2)d 1 on the viability of adult flies homozygous for this mutation. We have found that the viability of the mutant females is reduced, while that of the mutant males is not affected. In addition, the capacity of the mutant females to be inseminated is considerably reduced, whilst all the mutant males are able to inseminate females. These effects on females are suppressed by Sxl M1. However, the fat body cells of fl(2)d 1 homozygous females are able to synthesize yolk proteins at the restrictive temperature. We have also carried out, in males, a clonal analysis of fl(2)d 2, a mutation lethal in both sexes. We have found that the clones are fully viable. We conclude that the gene fl(2)d seems to be necessary during the adult life of females for the processes that require Sxl + activity. Moreover, the Sxl-independent vital function of fl(2)d seems to be required in both sexes only during larval development.

6 citations

Journal ArticleDOI
TL;DR: This short review of recent microscopic and chromosome conformation capture data that reveal key features of the compensated X chromosome and highlight the events leading to the establishment of a functional, specialized nuclear compartment, the X domain are summarized.

6 citations

Posted ContentDOI
09 Sep 2019-bioRxiv
TL;DR: It is shown that these beetles display a rare unequivocal example of the absence of a faster-X effect in a metazoan, and two potential causes are proposed, namely high constraint on X-linked ovary-biased genes, and an extreme lack of dosage compensation of genes transcribed in the testis.
Abstract: Background The faster-X effect, namely the rapid evolution of protein-coding genes on the X-chromosome, has been reported in numerous metazoans. However, the prevalence of this phenomenon across metazoans and its potential causes remain largely unresolved. Analysis of sex-biased genes may elucidate its possible mechanisms: a more pronounced faster-X effect in male-biased genes than in female-biased or unbiased genes, suggests fixation of recessive beneficial mutations rather than genetic drift. Further, theory predicts that the faster-X effect should be promoted by X-chromosome dosage compensation, but this topic remains rarely empirically examined. Results Here, we asked whether we could detect a faster-X effect in genes of the beetle Tribolium castaneum (and T. freemani orthologs), which has X/Y sex-determination and heterogametic males. Our comparison of protein sequence divergence (dN/dS) on the X-chromosome versus autosomes indicated the complete absence of a faster-X effect. Further, analyses of sex-biased gene expression revealed that the X-chromosome was strongly enriched for ovary-biased genes, which evolved under exceptionally high constraint. An evaluation of male X-chromosome dosage compensation in the gonads and in non-gonadal somatic tissues showed an extreme lack of compensation in the testis. This under-expression of the X chromosome in males may limit the phenotypic effect, and therefore likelihood of fixation, of recessive beneficial X-linked mutations in genes transcribed in male gonads. Conclusions We show that these beetles display a rare unequivocal example of the absence of a faster-X effect in a metazoan. We propose two potential causes for this, namely high constraint on X-linked ovary-biased genes, and an extreme lack of dosage compensation of genes transcribed in the testis.

6 citations


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