Evidence map›Paper›PMID 36808136›Full record

ArticleNature communications2023

Hypothesis-free phenotype prediction within a genetics-first framework.

Chang Lu, Jan Zaucha, Rihab Gam, Hai Fang, Ben Smithers, Matt E Oates, Miguel Bernabe-Rubio, James Williams, Natalie Zelenka, Arun Prasad Pandurangan and 8 more

Abstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

18 authors.

Chang LuMRC Laboratory of Molecular Biology, Cambridge Biomedical Campus, Francis Crick Avenue, Cambridge, CB2 0QH, UK.ORCID 0000-0002-3272-0120
Jan ZauchaDepartment of Computer Science, University of Bristol, Bristol, BS8 1UB, UK.
Rihab GamMRC Laboratory of Molecular Biology, Cambridge Biomedical Campus, Francis Crick Avenue, Cambridge, CB2 0QH, UK.
Hai FangDepartment of Computer Science, University of Bristol, Bristol, BS8 1UB, UK.
Ben SmithersDepartment of Computer Science, University of Bristol, Bristol, BS8 1UB, UK.
Matt E OatesDepartment of Computer Science, University of Bristol, Bristol, BS8 1UB, UK.
Miguel Bernabe-RubioCentre for Gene Therapy and Regenerative Medicine, King's College London, Guy's Hospital, Floor 28, Tower Wing, Great Maze Pond, London, SE1 9RT, UK.
James WilliamsCentre for Gene Therapy and Regenerative Medicine, King's College London, Guy's Hospital, Floor 28, Tower Wing, Great Maze Pond, London, SE1 9RT, UK.ORCID 0000-0003-3206-7851
Natalie ZelenkaDepartment of Computer Science, University of Bristol, Bristol, BS8 1UB, UK.ORCID 0000-0002-1007-0286
Arun Prasad PanduranganMRC Laboratory of Molecular Biology, Cambridge Biomedical Campus, Francis Crick Avenue, Cambridge, CB2 0QH, UK.ORCID 0000-0001-7168-7143
Himani TandonMRC Laboratory of Molecular Biology, Cambridge Biomedical Campus, Francis Crick Avenue, Cambridge, CB2 0QH, UK.
Hashem ShihabDepartment of Computer Science, University of Bristol, Bristol, BS8 1UB, UK.
Raju KalaivaniMRC Laboratory of Molecular Biology, Cambridge Biomedical Campus, Francis Crick Avenue, Cambridge, CB2 0QH, UK.
Minkyung SungMRC Laboratory of Molecular Biology, Cambridge Biomedical Campus, Francis Crick Avenue, Cambridge, CB2 0QH, UK.
Adam J SardarDepartment of Computer Science, University of Bristol, Bristol, BS8 1UB, UK.ORCID 0000-0002-6912-6125
Bastian Greshake TzovorasUniversité de Paris, INSERM U1284, Center for Research and Interdisciplinarity (CRI), Paris, France.ORCID 0000-0002-9925-9623
Davide DanoviCentre for Gene Therapy and Regenerative Medicine, King's College London, Guy's Hospital, Floor 28, Tower Wing, Great Maze Pond, London, SE1 9RT, UK.ORCID 0000-0003-4119-5337
Julian GoughMRC Laboratory of Molecular Biology, Cambridge Biomedical Campus, Francis Crick Avenue, Cambridge, CB2 0QH, UK. gough@mrc-lmb.cam.ac.uk.ORCID 0000-0002-1965-4982

Funding

Medical Research Council MC_EX_MR/S300005/1Medical Research Council MC_UP_1201/14Wellcome Trust
6 · The paper itself

Abstract

Cohort-wide sequencing studies have revealed that the largest category of variants is those deemed 'rare', even for the subset located in coding regions (99% of known coding variants are seen in less than 1% of the population. Associative methods give some understanding how rare genetic variants influence disease and organism-level phenotypes. But here we show that additional discoveries can be made through a knowledge-based approach using protein domains and ontologies (function and phenotype) that considers all coding variants regardless of allele frequency. We describe an ab initio, genetics-first method making molecular knowledge-based interpretations for exome-wide non-synonymous variants for phenotypes at the organism and cellular level. By using this reverse approach, we identify plausible genetic causes for developmental disorders that have eluded other established methods and present molecular hypotheses for the causal genetics of 40 phenotypes generated from a direct-to-consumer genotype cohort. This system offers a chance to extract further discovery from genetic data after standard tools have been applied.

Indexed as

ExomeGenetic Predisposition to DiseaseGene FrequencyGenotypeHumansPhenotype

Identifiers

PMID36808136
PMCPMC9938118

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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.