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: In the present review, the dynamics of modifications occurring during embryonic inactivation, their distribution over the inactive X-chromosome, interaction, and the role in establishing and maintening the inactive state are discussed.
Abstract: In female mammals, the process of dosage compensation occurs during early embryonic development. As a result of this, one of X-chromosomes becomes transcriptionally inactive. This process is accompanied by chromatin remodeling on inactivated X-chromosome, providing transcriptional silencing of the genes and maintenance of their inactive state. In the present review, the dynamics of modifications occurring during embryonic inactivation, their distribution over the inactive X-chromosome, interaction, and the role in establishing and maintening the inactive state are discussed. As an illustration, modifications on the inactive X-chromosome of the Microtus common vole are presented.
8 citations
TL;DR: Muller found halving gene dosage, as in males with one X chromosome, did not affect specific gene function, but why then was dosage "compensated?"
Abstract: Muller found halving gene dosage, as in males with one X chromosome, did not affect specific gene function. Why then was dosage "compensated?" This paradox was solved by invoking collective gene functions such as self/not self discrimination afforded by protein aggregation pressure. This predicts female susceptibility to autoimmune disease.
8 citations
TL;DR: It seems that despite the evolutionary diversification between these two species, the regulatory system which brings about the dosage compensation of X-chromosome activity has been conserved.
Abstract: We have used the unstable ring X-chromosome of D. melanogaster to generate XX/X0 mosaics in the hybrid progeny from crosses between D. melanogaster females and D. simulans males. The functional properties of the polytene X-chromosome(s) in salivary glands of such X0/XX mosaic hybrid larvae have been analysed by autoradiography after 3H-uridine or 3H-thymidine labelling of the glands. The simulans X-chromosome in the hybrid X0 nuclei displays typical pale staining, enlarged diameter, higher rate of transcription (nearly two times higher than each of the Xs in the XX nuclei in the same gland) and a faster completion of replication as would be the case in the original parental X0 or XY nuclei. In the hybrid XX polytene nuclei, the melanogaster as well as the simulans X functions in the same manner as in female cells of the parents. The nucleolar transcription is also equal in the hybrid XX and X0 nuclei. Thus is seems that despite the evolutionary diversification between these two species, the regulator system which brings about the dosage compensation of X-chromosome activity has been conserved.
8 citations
TL;DR: D dosage compensation operates in the An.
Abstract: Dosage compensation has evolved in concert with Y-chromosome degeneration in many taxa that exhibit heterogametic sex chromosomes. Dosage compensation overcomes the biological challenge of a "half dose" of X chromosome gene transcripts in the heterogametic sex. The need to equalize gene expression of a hemizygous X with that of autosomes arises from the fact that the X chromosomes retain hundreds of functional genes that are actively transcribed in both sexes and interact with genes expressed on the autosomes. Sex determination and heterogametic sex chromosomes have evolved multiple times in Diptera, and in each case the genetic control of dosage compensation is tightly linked to sex determination. In the Anopheles gambiae species complex (Culicidae), maleness is conferred by the Y-chromosome gene Yob, which despite its conserved role between species is polymorphic in its copynumber between them. Previous work demonstrated that male An.gambiae s.s. males exhibit complete dosage compensation in pupal and adult stages. In the present study, we have extended this analysis to three sister species in the An. gambiae complex: An. coluzzii, An. arabiensis, and An. quadriannulatus. In addition, we analyzed dosage compensation in bi-directional F1 hybrids between these species to determine if hybridization results in the mis-regulation and disruption of dosage compensation. Our results confirm that dosage compensation operates in the An. gambiae species complex through the hypertranscription of the male X chromosome. Additionally, dosage compensation in hybrid males does not differ from parental males, indicating that hybridization does not result in the mis-regulation of dosage compensation.
8 citations
TL;DR: There is some evidence to suggest that the sex hormones, rather than a specific sex-linked gene with a dosage effect similar to that of B, are responsible for autosexing in non-barred breeds, but on whether the testicular or the ovarian hormone is responsible the available evidence is conflicting.
Abstract: 1.
Autosexing breeds of fowl may be divided into those which carry the sex-linked gene for barring (B), and those which do not. In the former group, the autosexing properties are due to the imperfect dominance of B.
2.
A table (Table 2) is presented showing the possible dominance relations between a sex-linked gene which is a hypomorph, hypermorph, antimorph, amorph or neomorph, and its wild-type allele, both without dosage compensation, and in conditions of partial and full dosage compensation.
3.
A study of the ‘ticks’occurring on birds having various constitutions for the two sex-linked loci B and S silver) shows that the ticks are due to somatic elimination of part of an X-chromosome. It shows further that B is a neomorph (b having no action on pigmentation) without dosage compensation, or possibly a hypomorph (b having a very weak action in the same direction as B) with, at most, a slight degree of dosage compensation. This in itself is sufficient to explain the autosexing properties of barred breeds, without resorting to the improbable assumption that females have a Y-chromosome which carries b.
4.
Anomalies are pointed out in the dominance relations at several sex-linked loci (w, A, B, Hw) ofDrosophila melanogaster, which are difficult to explain on Muller’s theory of dosage compensation.
5.
There is no reason to attribute any autosexing effect to either allele at the silver locus of the fowl. There is some evidence to suggest that the sex hormones, rather than a specific sex-linked gene with a dosage effect similar to that of B, are responsible for autosexing in non-barred breeds. On whether the testicular or the ovarian hormone is responsible, the available evidence is conflicting.
8 citations