Evidence map›Paper›PMID 40601579›Full record

ArticlePLoS genetics2025

Phenotypic tolerance for rDNA copy number variation within the natural range of C. elegans.

Ashley N Hall, Elizabeth A Morton, Rebecca Walters, Josh T Cuperus, Christine Queitsch

Abstract read
In one paragraph

Article in PLoS genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Ashley N HallMolecular and Cellular Biology Program, University of Washington, Seattle, Washington, United States of America.ORCID https://orcid.org/0000-0001-7739-1706
Elizabeth A MortonDepartment of Biology, SUNY Brockport, Brockport, New York, United States of America.ORCID https://orcid.org/0000-0003-3451-4950
Rebecca WaltersDepartment of Biology, SUNY Brockport, Brockport, New York, United States of America.ORCID https://orcid.org/0009-0002-7278-0432
Josh T CuperusDepartment of Genome Sciences, University of Washington, Seattle, Washington, United States of America.ORCID https://orcid.org/0000-0002-8019-7733
Christine QueitschDepartment of Genome Sciences, University of Washington, Seattle, Washington, United States of America.ORCID https://orcid.org/0000-0002-0905-4705

Funding

Technology to understand genetic variant effects in contextRM1HG010461 · NHGRI · UNIVERSITY OF WASHINGTON · PI Douglas M Fowler, Bruce Colston Trapnell · 2019 to 2026
$18.9M
Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
Understanding gene regulation in contextR35GM139532 · NIGMS · UNIVERSITY OF WASHINGTON · PI Christine Queitsch · 2021 to 2026
$3.3M
Ribosomal DNA copy number variation as a source of missing heritability in complex traitsR01GM122088 · NIGMS · UNIVERSITY OF WASHINGTON · PI QUEITSCH, CHRISTINE · 2017 to 2019
$1.4M
Determining the role of ribosomal DNA in metazoan agingF31AG063450 · NIA · UNIVERSITY OF WASHINGTON · PI HALL, ASHLEY NICOLE · 2019 to 2020
$79k
NHGRI NIH HHS RM1 HG010461NIA NIH HHS F31 AG063450NIGMS NIH HHS R01 GM122088NIGMS NIH HHS R35 GM139532NIH HHS P40 OD010440
6 · The paper itself

Abstract

The genes for ribosomal RNA (rRNA) are encoded by ribosomal DNA (rDNA), whose structure is notable for being present in arrays of tens to thousands of tandemly repeated copies in eukaryotic genomes. The exact number of rDNA copies per genome is highly variable within a species, with differences between individuals measuring in potentially hundreds of copies and megabases of DNA. The extent to which natural variation in rDNA copy number impacts whole-organism phenotypes such as fitness and lifespan is poorly understood, in part due to difficulties in manipulating such large and repetitive tracts of DNA even in model organisms. Here, we used the natural resource of copy number variation in C. elegans wild isolates to generate new tools and investigated the phenotypic consequences of this variation. Specifically, we generated a panel of recombinant inbred lines (RILs) using a laboratory strain derivative with ~130 haploid rDNA copies and a wild isolate with ~417 haploid rDNA copies, one of the highest validated C. elegans rDNA copy number arrays. We find that rDNA copy number is stable in the RILs, rejecting prior hypotheses that predicted copy number instability and copy number reversion. To isolate effects of rDNA copy number on phenotype, we produced a series of near isogenic lines (NILs) with rDNA copy numbers representing the high and low end of the rDNA copy number spectrum in C. elegans wild isolates. We find no correlation between rDNA copy number and phenotypes of rRNA abundance, competitive fitness, early life fertility, lifespan, or global transcriptome under standard laboratory conditions. These findings demonstrate a remarkable ability of C. elegans to tolerate substantial variation in a locus critical to fundamental cell function. Our study provides strain resources for future investigations into the boundaries of this tolerance.

Indexed as

Caenorhabditis elegansDNA Copy Number VariationsDNA, RibosomalAnimalsLongevityPhenotypeDNA, Ribosomal

Identifiers

PMID40601579
PMCPMC12221044

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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.