Evidence map›Paper›PMID 38645217›Full record

ArticlebioRxiv : the preprint server for biology2024

Recalibrating differential gene expression by genetic dosage variance prioritizes functionally relevant genes.

Philipp Rentzsch, Aaron Kollotzek, Pejman Mohammadi, Tuuli Lappalainen

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors.

Philipp RentzschScience for Life Laboratory, Department of Gene Technology, KTH Royal Institute of Technology, Solna, Sweden.ORCID 0000-0002-0413-7974
Aaron KollotzekScience for Life Laboratory, Department of Gene Technology, KTH Royal Institute of Technology, Solna, Sweden.
Pejman MohammadiCenter for Immunity and Immunotherapies, Seattle Children's Research Institute, Seattle, WA, USA; Department of Pediatrics, University of Washington School of Medicine, Seattle, WA, USA; Department of Genome Science, University of Washington, Seattle, WA, USA.ORCID 0000-0003-4457-8552
Tuuli LappalainenScience for Life Laboratory, Department of Gene Technology, KTH Royal Institute of Technology, Solna, Sweden.ORCID 0000-0002-7746-8109

Funding

Haplotype-aware models of gene and isoform expression with application to genetic studies of disease in diverse populationsR01GM140287 · NIGMS · SEATTLE CHILDREN'S HOSPITAL · PI GAMAZON, ERIC R, MOHAMMADI, PEJMAN · 2021 to 2024
$2.8M
NIGMS NIH HHS R01 GM140287
6 · The paper itself

Abstract

Differential expression (DE) analysis is a widely used method for identifying genes that are functionally relevant for an observed phenotype or biological response. However, typical DE analysis includes selection of genes based on a threshold of fold change in expression under the implicit assumption that all genes are equally sensitive to dosage changes of their transcripts. This tends to favor highly variable genes over more constrained genes where even small changes in expression may be biologically relevant. To address this limitation, we have developed a method to recalibrate each gene's differential expression fold change based on genetic expression variance observed in the human population. The newly established metric ranks statistically differentially expressed genes not by nominal change of expression, but by relative change in comparison to natural dosage variation for each gene. We apply our method to RNA sequencing datasets from rare disease and in-vitro stimulus response experiments. Compared to the standard approach, our method adjusts the bias in discovery towards highly variable genes, and enriches for pathways and biological processes related to metabolic and regulatory activity, indicating a prioritization of functionally relevant driver genes. With that, our method provides a novel view on DE and contributes towards bridging the existing gap between statistical and biological significance. We believe that this approach will simplify the identification of disease causing genes and enhance the discovery of therapeutic targets.

Identifiers

PMID38645217
PMCPMC11030425

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.