Evidence map›Paper›PMID 28132849›Full record

ArticleDevelopmental cell2017

Non-Canonical and Sexually Dimorphic X Dosage Compensation States in the Mouse and Human Germline.

Mahesh N Sangrithi, Helene Royo, Shantha K Mahadevaiah, Obah Ojarikre, Leena Bhaw, Abdul Sesay, Antoine H F M Peters, Michael Stadler, James M A Turner

Open access · hybridAbstract read
In one paragraph

Article in Developmental cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
8.1field-weighted citation impact, top 2% of its field
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

54 citing papers in PubMed, 108 citations in OpenAlex.

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  11. Genome-wide DNA methylation changes in human spermatogenesis.American journal of human genetics · 2024
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  13. RNA stability controlled by mNature structural & molecular biology · 2023
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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

9 authors at 3 institutions in 2 countries.

Mahesh N SangrithiMill Hill Laboratory, The Francis Crick Institute, The Ridgeway, Mill Hill, London NW7 1AA, UK; UCL EGA Institute for Women's Health UCL, Medical School Building, 74 Huntley Street, London WC1E 6AU, UK.
Helene RoyoFriedrich Miescher Institute for Biomedical Research (FMI), 4058 Basel, Switzerland; Swiss Institute of Bioinformatics, 4058 Basel, Switzerland.
Shantha K MahadevaiahMill Hill Laboratory, The Francis Crick Institute, The Ridgeway, Mill Hill, London NW7 1AA, UK.
Obah OjarikreMill Hill Laboratory, The Francis Crick Institute, The Ridgeway, Mill Hill, London NW7 1AA, UK.
Leena BhawMill Hill Laboratory, The Francis Crick Institute, The Ridgeway, Mill Hill, London NW7 1AA, UK.
Abdul SesayMill Hill Laboratory, The Francis Crick Institute, The Ridgeway, Mill Hill, London NW7 1AA, UK.
Antoine H F M PetersFriedrich Miescher Institute for Biomedical Research (FMI), 4058 Basel, Switzerland.
Michael StadlerFriedrich Miescher Institute for Biomedical Research (FMI), 4058 Basel, Switzerland; Swiss Institute of Bioinformatics, 4058 Basel, Switzerland.
James M A TurnerMill Hill Laboratory, The Francis Crick Institute, The Ridgeway, Mill Hill, London NW7 1AA, UK. Electronic address: james.turner@crick.ac.uk.
The Francis Crick Institute · GBFriedrich Miescher Institute · CHSIB Swiss Institute of Bioinformatics · CH

Funding

Medical Research Council U117588498Wellcome Trust
6 · The paper itself

Abstract

Somatic X dosage compensation requires two mechanisms: X inactivation balances X gene output between males (XY) and females (XX), while X upregulation, hypothesized by Ohno and documented in vivo, balances X gene with autosomal gene output. Whether X dosage compensation occurs in germ cells is unclear. We show that mouse and human germ cells exhibit non-canonical X dosage states that differ from the soma and between the sexes. Prior to genome-wide reprogramming, X upregulation is present, consistent with Ohno's hypothesis. Subsequently, however, it is erased. In females, erasure follows loss of X inactivation, causing X dosage excess. Conversely, in males, erasure leads to permanent X dosage decompensation. Sex chromosomally abnormal models exhibit a "sex-reversed" X dosage state: XX males, like XX females, develop X dosage excess, while XO females, like XY males, develop X dosage decompensation. Thus, germline X dosage compensation states are determined by X chromosome number, not phenotypic sex. These unexpected differences in X dosage compensation states between germline and soma offer unique perspectives on sex chromosome infertility.

Indexed as

Dosage Compensation, GeneticSex CharacteristicsAnimalsCellular ReprogrammingChromosomes, Human, XDatabases, GeneticFemaleGene Expression ProfilingGene Expression RegulationGerm CellsGonadsHumansMaleMiceModels, GeneticSequence Analysis, RNAdosage compensationgenome-wide reprogramminggermline developmentsex chromosomesX inactivationX upregulation

Identifiers

PMID28132849
PMCPMC5300051
OpenAlexW2582005133

What OpenQuestion holds

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LicenceCC BY
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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.