Evidence map›Paper›PMID 35994124›Full record

ArticleHuman genetics2023

Hemizygosity can reveal variant pathogenicity on the X-chromosome.

Timothy H Ciesielski, Jacquelaine Bartlett, Sudha K Iyengar, Scott M Williams

Open access · greenAbstract read
In one paragraph

Article in Human genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
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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

4 authors at 2 institutions in 1 country.

Timothy H CiesielskiThe Department of Population and Quantitative Health Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
Jacquelaine BartlettThe Department of Population and Quantitative Health Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
Sudha K IyengarThe Department of Population and Quantitative Health Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
Scott M WilliamsThe Department of Population and Quantitative Health Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, USA. smw154@case.edu.
Case Western Reserve University · USRonin Institute · US

Funding

TISSUE CULTURE AND HYBRIDOMA MODULEP30EY011373 · NEI · CASE WESTERN RESERVE UNIVERSITY · PI Irina A Pikuleva · 1997 to 2026
$17.7M
Bioinformatics Strategies for Genome-Wide Association StudiesR01LM010098 · NLM · UNIVERSITY OF PENNSYLVANIA · PI MOORE, JASON H., WILLIAMS, SCOTT MATTHEW · 2009 to 2023
$5.1M
Primaquine metabolism and treatment of P. vivax in MadagascarR01AI148469 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI WILLIAMS, SCOTT MATTHEW, ZIMMERMAN, PETER A. · 2020 to 2023
$2.6M
NEI NIH HHS EY011373NEI NIH HHS P30 EY011373NIAID NIH HHS R01 AI148469NLM NIH HHS R01 LM010098U.S. National Library of Medicine LM010098
6 · The paper itself

Abstract

Pathogenic variants on the X-chromosome can have more severe consequences for hemizygous males, while heterozygote females can avoid severe consequences due to diploidy and the capacity for nonrandom expression. Thus, when an allele is more common in females this could indicate that it increases the probability of early death in the male hemizygous state, which can be considered a measure of pathogenicity. Importantly, large-scale genomic data now makes it possible to compare allele proportions between the sexes. To discover pathogenic variants on the X-chromosome, we analyzed exome data from 125,748 ancestrally diverse participants in the Genome Aggregation Database (gnomAD). After filtering out duplicates and extremely rare variants, 44,606 of the original 348,221 remained for analysis. We divided the proportion of variant alleles in females by the proportion in males for all variant sites, and then placed each variant into one of three a priori categories: (1) Reference (Primarily synonymous and intronic), (2) Unlikely-to-be-tolerated (Primarily missense), and (3) Least-likely-to-be-tolerated (Primarily frameshift). To assess the impact of ploidy, we compared the distribution of these ratios between pseudoautosomal and non-pseudoautosomal regions. In the non-pseudoautosomal regions, mean female-to-male ratios were lowest among Reference (2.40), greater for Unlikely-to-be-tolerated (2.77) and highest for Least-likely-to-be-tolerated (3.28) variants. Corresponding ratios were lower in the pseudoautosomal regions (1.52, 1.57, and 1.68, respectively), with the most extreme ratio being just below 11. Because pathogenic effects in the pseudoautosomal regions should not drive ratio increases, this maximum ratio provides an upper bound for baseline noise. In the non-pseudoautosomal regions, 319 variants had a ratio over 11. In sum, we identified a measure with a dataset specific threshold for identifying pathogenicity in non-pseudoautosomal X-chromosome variants: the female-to-male allele proportion ratio.

Indexed as

ExomeHeterozygoteX ChromosomeChromosomesFemaleHumansMaleVirulence

Identifiers

PMID35994124
PMCPMC9840679
OpenAlexW4292608150

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Registered trials

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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.