Dosage compensation articles within Nature Communications

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  • Article
    | Open Access

    Here the authors investigate the functional relevance of X-chromosome inactivation (XCI) regulator Xist in hematopoiesis. They find that Xist loss leads to changes in the ratio of hematopoietic progenitor cells and results in chromatin accessibility and transcriptional upregulation on the inactive X chromosome, including XCI escape genes known to be associated with cell cycle and immune response.

    • Tianqi Yang
    • , Jianhong Ou
    •  & Eda Yildirim

  • Article
    | Open Access

    Here the authors investigate whether for imprinted genes the parent-of-origin of the expressed allele or rather appropriate gene dosage is more important for normal development. Using the differentially methylated region of Dlk1-Dio3 gene involved in imprinting, they show that correct parent-of-origin imprinting pattern is secondary to balanced gene dosage.

    • Ariella Weinberg-Shukron
    • , Raz Ben-Yair
    •  & Yonatan Stelzer

  • Article
    | Open Access

    The concerted dynamics of X-chromosome upregulation and X-chromosome inactivation, which collectively balance X-chromosome expression, are not well understood. Using allelic single-cell genomics, the authors characterize the dynamics of X-chromosome upregulation and inactivation along mouse embryonic and stem cell development, calling to question keys aspects of the established model of mammalian dosage compensation.

    • Antonio Lentini
    • , Huaitao Cheng
    •  & Björn Reinius

  • Article
    | Open Access

    Both A/B compartments and TADs are thought to be absent from the inactive X chromosome, but to be re-established with transcriptional reactivation and chromatin opening during X-reactivation. Here, the authors characterise gene reactivation, chromatin opening and chromosome topology during X-reactivation, observe A/B-like compartments on the inactive X that guide TAD formation independently of transcription during X-reactivation.

    • Moritz Bauer
    • , Enrique Vidal
    •  & Bernhard Payer

  • Article
    | Open Access

    In Drosophila, dosage compensation involves a twofold transcriptional upregulation of the single male chromosome X. Here the authors show that global conformational differences are specifically present in the male X chromosome and detectable using Hi-C data, indicating that dosage compensation affects global chromosome structure.

    • Koustav Pal
    • , Mattia Forcato
    •  & Francesco Ferrari

  • Article
    | Open Access

    Skewing of X chromosome inactivation (XCI) occurs when the silencing of one parental X chromosome is non-random. Here, Zito et al. report XCI patterns in lymphoblastoid cell lines, blood, subcutaneous adipose tissue samples and skin samples of monozygotic and dizygotic twins and find XCI skew to associate with tissue and age.

    • Antonino Zito
    • , Matthew N. Davies
    •  & Kerrin S. Small

  • Article
    | Open Access

    The position, shape and number of transcription start sites (TSS) regulate gene expression. Here authors present MAPCap, a method for high-resolution detection and differential expression analysis of TSS, and apply MAPCap to early fly development, detecting stage and sex-specific promoter and enhancer activity.

    • Vivek Bhardwaj
    • , Giuseppe Semplicio
    •  & Asifa Akhtar

  • Article
    | Open Access

    Dosage compensation (DC) on the X chromosome has predictable effects on genetic and phenotypic trait variance. Here, the authors use information for 20 quantitative traits in the UK Biobank and across-tissue gene expression to compare X-linked heritability and the effects of trait-associated SNPs between the sexes.

    • Julia Sidorenko
    • , Irfahan Kassam
    •  & Peter M. Visscher

  • Article
    | Open Access

    The inactive X chromosome (Xi) has an atypical structure, with global loss of TADs, A/B compartments and formation of mega-domains. Here the authors show that the non-canonical SMC family protein, SmcHD1, important for developmental gene silencing on Xi, antagonises TAD formation and compartmentalization on the Xi in a transcription independent way.

    • Michal R. Gdula
    • , Tatyana B. Nesterova
    •  & Neil Brockdorff

  • Article
    | Open Access

    The mammalian inactive X-chromosome (Xi) is organized into megadomains and superloops directed by the noncoding loci, Dxz4 and Firre. Here the authors provide evidence that megadomains do not precede Xist expression or Xi gene silencing, and suggest that Dxz4, Firre, and megadomains are dispensable for Xi silencing and escape from X-inactivation.

    • John E. Froberg
    • , Stefan F. Pinter
    •  & Jeannie T. Lee

  • Article
    | Open Access

    REX1 has been shown to regulate pluripotency of ESCs, genomic imprinting and preimplantation development in mice. Here the authors provide evidence that REX1 is the prime target of RNF12 E3 ubiquitin ligase and that Rex1 removal rescues the Rnf12 knockout phenotype in imprinted X chromosome inactivation in mice.

    • Cristina Gontan
    • , Hegias Mira-Bontenbal
    •  & Joost Gribnau

  • Article
    | Open Access

    Although Ftx lncRNA has been linked to X-chromosome inactivation, its physiological roles in vivo remain unclear. Here the authors show that deletion of mouse Ftx causes eye abnormalities similar to human microphthalmia in a subset of female mice but rarely in males and provide evidence that Ftx plays a role in gene silencing on the inactive X chromosome.

    • Yusuke Hosoi
    • , Miki Soma
    •  & Shin Kobayashi

  • Article
    | Open Access

    In Drosophila the Male-Specific Lethal complex (MSLc) mediates upregulation of the single male X chromosome. Here the authors provide evidence that MSL2 also targets autosomal genes required for proper development and that MSL2 binds and similarly regulates mouse orthologues.

    • Claudia Isabelle Keller Valsecchi
    • , M. Felicia Basilicata
    •  & Asifa Akhtar

  • Article
    | Open Access

    The inactive X chromosome condenses into a bipartite structure. Here the authors use cells with allelic deletions or inversions to show that the Dxz4 locus is necessary to maintain the bipartite structure and that Dxz4 orientation controls the distribution of contacts on the inactive X chromosome.

    • G. Bonora
    • , X. Deng
    •  & C. M. Disteche

  • Article
    | Open Access

    X-chromosome inactivation is reversed in the mouse inner cell mass (ICM) through a mechanism that is not fully understood. Here, the authors investigate this process and characterize the contributions of the epigenetic landscape and transcription factors in X-linked gene reactivation dynamics.

    • Maud Borensztein
    • , Ikuhiro Okamoto
    •  & Edith Heard

  • Article
    | Open Access

    Xist RNA is required for X chromosome inactivation but it is not well understood how Xist silences some regions more efficiently than others. Here, the authors induce ectopic Xist expression from multiple different X-linked and autosomal loci in cells to explore Xist function.

    • Agnese Loda
    • , Johannes H. Brandsma
    •  & Joost Gribnau

  • Article
    | Open Access

    Complete sex chromosome dosage compensation is largely limited to male heterogametic species, with the majority of female heterogametic species displaying incomplete dosage compensation. Here, the authors show that sexual conflict over gene expression combined with sexual selection in males can explain this pattern.

    • Charles Mullon
    • , Alison E. Wright
    •  & Judith E. Mank

  • Article
    | Open Access

    During mouse preimplantation phases, a repressive imprint is imposed on the maternal allele of Xist, which encodes a large non-coding RNA required for X-chromosome inactivation. Here the authors show that trimethylation of histone H3 at lysine 9 on Xist promoter chromatin is responsible for the maternally determined Xistrepression.

    • Atsushi Fukuda
    • , Junko Tomikawa
    •  & Akihiro Umezawa

  • Article |

    X-chromosome inactivation is a tightly regulated mechanism, which silences one of the two female X chromosomes. Here Makhlouf et al. show that the autosomal transcription factor YY1 directly promotes expression of the XistRNA—a master regulator of X-chromosome inactivation—at the onset of the inactivation process.

    • Mélanie Makhlouf
    • , Jean-François Ouimette
    •  & Claire Rougeulle

  • Article |

    The process that balances expression of X-chromosomal genes between males and females is under tight regulatory control. Here, Militti et al. show that in Drosophila, the RNA-binding protein UNR functions during dosage compensation to promote the interaction between the RNA helicase MLE and the long non-coding RNA roX2.

    • Cristina Militti
    • , Sylvain Maenner
    •  & Fátima Gebauer

  • Article |

    Imprinted mouse X-chromosome inactivation is controlled by two long non-coding RNAs, Tsix and Xist. Here, Maclary et al. demonstrate that Tsix is dispensable during the initiation and maintenance of X-inactivation in vivo and in vitro, but required to prevent Xist expression as trophectodermal progenitors differentiate.

    • Emily Maclary
    • , Emily Buttigieg
    •  & Sundeep Kalantry

  • Article
    | Open Access

    How one copy of the X chromosome is silenced in replicating female somatic cells is poorly understood. Here, the authors demonstrate that the inactive X chromosome is replicated before constitutive heterochromatin and that histone hypoacetylation has a role in controlling replication of the inactive X chromosome.

    • Corella S. Casas-Delucchi
    • , Alessandro Brero
    •  & M. Cristina Cardoso

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