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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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TL;DR: The main difference between the two sexes is an elevation in X chromosome expression in females relative to males signifying incomplete dosage compensation with a few select genes exhibiting even higher expression increases, which indicate that the male program is the default mode in the germline that is driven to female development with a second X chromosome.
Abstract: Germ cells in D. melanogaster are specified maternally shortly after fertilization and are transcriptionally quiescent until their zygotic genome is activated to sustain further development. To understand the molecular basis of this process, we analyzed the progressing transcriptomes of early male and female germ cells at the single-cell level between germline specification and coalescence with somatic gonadal cells. Our data comprehensively covered zygotic activation in the germline genome, and analyses on genes that exhibit germline-restricted expression revealed that polymerase pausing and differential RNA stability are important mechanisms that establish gene expression differences between the germline and soma. In addition, we observed an immediate bifurcation between the male and female germ cells as zygotic transcription begins. The main difference between the two sexes is an elevation in X chromosome expression in females relative to males signifying incomplete dosage compensation with a few select genes exhibiting even higher expression increases. These indicate that the male program is the default mode in the germline that is driven to female development with a second X chromosome.
TL;DR: In this paper, the Drosophila Individual Activity Monitoring and Detecting System (DIAMonDS) was used to detect the precise timing of both pupariation and eclosion of individual flies.
Abstract: Many animal species exhibit sex differences in the time period prior to reaching sexual maturity. However, the underlying mechanism for such biased maturation remains poorly understood. Females of the fruit fly Drosophila melanogaster eclose 4 h faster on average than males, owing to differences in the pupal period between the sexes; this characteristic is referred to as the protogyny phenotype. Here, we aimed to elucidate the mechanism underlying the protogyny phenotype in the fruit fly using our newly developed Drosophila Individual Activity Monitoring and Detecting System (DIAMonDS), which can continuously detect the precise timing of both pupariation and eclosion of individual flies. Via this system, following the laying of eggs, we detected the precise time points of pupariation and eclosion of a large number of individual flies simultaneously and succeeded in identifying the tiny differences in pupal duration between females and males. We first explored the role of physiological sex by establishing transgender flies via knockdown of the sex-determination gene, transformer (tra) and its co-factor tra2, which retained the protogyny phenotype. In addition, disruption of dosage compensation by male-specific lethal (msl-2) knockdown did not affect the protogyny phenotype. The Drosophila master sex switch gene--Sxl promotes female differentiation via tra and turns off male dosage compensation through the repression of msl-2. However, we observed that stage-specific whole-body knockdown and mutation of Sxl induced disturbance of the protogyny phenotype. These results suggest that an additional, non-canonical function of Sxl involves establishing the protogyny phenotype in D. melanogaster. Author summaryA wide variety of animals show differences in time points of sexual maturation between sexes. For example, in many mammals, including human beings, females mature faster than males. This maturation often takes several months or years, and precisely detecting the time point of maturation is challenging, because of the continuity of growth, especially in mammals. Moreover, the reason behind the difference in sexual maturation time points between sexes is not fully understood. The fruit fly Drosophila--a model organism--also shows biased maturation between the sexes, with females emerging 4 h faster than males (a characteristic known as the protogyny phenotype). To understand the mechanism underlying the protogyny phenotype, we used our newly developed system, Drosophila Individual Activity Monitoring and Detecting System (DIAMonDS), to detect the precise eclosion point in individual fruit flies. Surprisingly, our analysis of transgender flies obtained by knockdown and overexpression techniques indicated that a physiological gender might not be necessary requirement for protogyny and that a non-canonical novel function of the fruit fly master sex switch gene, Sxl, regulates protogyny in fruit flies.
TL;DR: Two recent studies identify an RNA-binding protein, UNR, as a novel corepressor that is recruited by SXL to the 3′ UTR of msl-2 mRNA for translation inhibition in females.
Abstract: Translational inhibition of male-specific msl-2 messenger RNA by the female-specific protein SXL is crucial for X-chromosome dosage compensation in Drosophila melanogaster. Two recent studies identify an RNA-binding protein, UNR, as a novel corepressor that is recruited by SXL to the 3' UTR of msl-2 mRNA for translation inhibition in females.
05 Dec 2022
TL;DR: In this paper , the authors compared the X-chromosome target specificity and mode of binding for the specialized condensin dosage compensation complex (DCC) controlling X expression between C briggsae (Cbr) and C. elegans (CEL).
Abstract: Abstract An evolutionary perspective enhances our understanding of biological mechanisms. Comparison of sex determination and X-chromosome dosage compensation mechanisms between the closely related nematode species C. briggsae ( Cbr ) and C. elegans ( Cel ) revealed that the genetic regulatory hierarchy controlling both processes is conserved, but the X-chromosome target specificity and mode of binding for the specialized condensin dosage compensation complex (DCC) controlling X expression have diverged. We identified two motifs within Cbr DCC recruitment sites that are highly enriched on X: 13-bp MEX and 30-bp MEX II. Mutating either MEX or MEX II in an endogenous recruitment site with multiple copies of one or both motifs reduced binding, but only removing all motifs eliminated binding in vivo . Hence, DCC binding to Cbr recruitment sites appears additive. In contrast, DCC binding to Cel recruitment sites is synergistic: mutating even one motif in vivo eliminated binding. Although all X-chromosome motifs share the sequence CAGGG, they have otherwise diverged so that a motif from one species cannot function in the other. Functional divergence was demonstrated in vivo and in vitro . A single nucleotide position in Cbr MEX can determine whether Cel DCC binds. This rapid divergence of DCC target specificity could have been an important factor in establishing reproductive isolation between nematode species and contrasts dramatically with conservation of target specificity for X-chromosome dosage compensation across Drosophila species and for transcription factors controlling developmental processes such as body-plan specification from fruit flies to mice.
TL;DR: In this paper , the authors compared the X-chromosome target specificity and mode of binding for the specialized condensin dosage compensation complex (DCC) controlling X expression.
Abstract: An evolutionary perspective enhances our understanding of biological mechanisms. Comparison of sex determination and X-chromosome dosage compensation mechanisms between the closely related nematode species Caenorhabditis briggsae (Cbr) and Caenorhabditis elegans (Cel) revealed that the genetic regulatory hierarchy controlling both processes is conserved, but the X-chromosome target specificity and mode of binding for the specialized condensin dosage compensation complex (DCC) controlling X expression have diverged. We identified two motifs within Cbr DCC recruitment sites that are highly enriched on X: 13 bp MEX and 30 bp MEX II. Mutating either MEX or MEX II in an endogenous recruitment site with multiple copies of one or both motifs reduced binding, but only removing all motifs eliminated binding in vivo. Hence, DCC binding to Cbr recruitment sites appears additive. In contrast, DCC binding to Cel recruitment sites is synergistic: mutating even one motif in vivo eliminated binding. Although all X-chromosome motifs share the sequence CAGGG, they have otherwise diverged so that a motif from one species cannot function in the other. Functional divergence was demonstrated in vivo and in vitro. A single nucleotide position in Cbr MEX can determine whether Cel DCC binds. This rapid divergence of DCC target specificity could have been an important factor in establishing reproductive isolation between nematode species and contrasts dramatically with the conservation of target specificity for X-chromosome dosage compensation across Drosophila species and for transcription factors controlling developmental processes such as body-plan specification from fruit flies to mice.