Evidence map›Paper›PMID 27542829›Full record

ArticleGenes & development2016

Female mice lacking Xist RNA show partial dosage compensation and survive to term.

Lin Yang, James E Kirby, Hongjae Sunwoo, Jeannie T Lee

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
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  10. Loss of XIST lncRNA unlocks stemness and cellular plasticity in ovarian cancer.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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  12. Review
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  18. Roles of the Rlim-Rex1 axis during X chromosome inactivation in mice.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  19. [LncRNA LINC00342 regulates gastric cancer cell proliferation, migration and invasion by targeting miR-596].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

Lin YangHoward Hughes Medical Institute, Massachusetts General Hospital, Boston, Massachusetts 02114, USA; Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA; Department of Genetics, Harvard Medical School, Boston, Massachusetts 02114, USA;
James E KirbyDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02114, USA.
Hongjae SunwooHoward Hughes Medical Institute, Massachusetts General Hospital, Boston, Massachusetts 02114, USA; Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA; Department of Genetics, Harvard Medical School, Boston, Massachusetts 02114, USA;
Jeannie T LeeHoward Hughes Medical Institute, Massachusetts General Hospital, Boston, Massachusetts 02114, USA; Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA; Department of Genetics, Harvard Medical School, Boston, Massachusetts 02114, USA;
Howard Hughes Medical Institute · USBeth Israel Deaconess Medical Center · USHarvard University · US

Funding

The RNA-activation platform to treat X-linked disease in a locus-specific manner.R01DA036895 · NIDA · MASSACHUSETTS GENERAL HOSPITAL · PI LEE, JEANNIE T · 2013 to 2017
$1.7M
NIDA NIH HHS R01 DA036895
6 · The paper itself

Abstract

X-chromosome inactivation (XCI) compensates for differences in X-chromosome number between male and female mammals. XCI is orchestrated by Xist RNA, whose expression in early development leads to transcriptional silencing of one X chromosome in the female. Knockout studies have established a requirement for Xist with inviability of female embryos that inherit an Xist deletion from the father. Here, we report that female mice lacking Xist RNA can, surprisingly, develop and survive to term. Xist-null females are born at lower frequency and are smaller at birth, but organogenesis is mostly normal. Transcriptomic analysis indicates significant overexpression of hundreds of X-linked genes across multiple tissues. Therefore, Xist-null mice can develop to term in spite of a deficiency of dosage compensation. However, the degree of X-autosomal dosage imbalance was less than anticipated (1.14-fold to 1.36-fold). Thus, partial dosage compensation can be achieved without Xist, supporting the idea of inherent genome balance. Nevertheless, to date, none of the mutant mice has survived beyond weaning stage. Sudden death is associated with failure of postnatal organ maturation. Our data suggest Xist-independent mechanisms of dosage compensation and demonstrate that small deviations from X-autosomal balance can have profound effects on overall fitness.

Indexed as

AnimalsDosage Compensation, GeneticEmbryonic DevelopmentFemaleGene Expression Regulation, DevelopmentalMaleMiceMyocardiumRNA, Long NoncodingSequence DeletionSpleenSurvival AnalysisX ChromosomeX Chromosome InactivationRNA, Long NoncodingXIST non-coding RNAdosage compensationgenome balanceinverse effectknockout mousetranscriptomicsX inactivationXist

Identifiers

PMID27542829
PMCPMC5002979
OpenAlexW2517978842

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.