Evidence map›Paper›PMID 39300074›Full record

ArticleNature communications2024

Multiple distinct evolutionary mechanisms govern the dynamics of selfish mitochondrial genomes in Caenorhabditis elegans.

Bryan L Gitschlag, Claudia V Pereira, James P Held, David M McCandlish, Maulik R Patel

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

5 authors.

Bryan L GitschlagDepartment of Biological Sciences, Vanderbilt University, Nashville, TN, USA. gitschl@cshl.edu.ORCID 0000-0002-7096-2147
Claudia V PereiraDepartment of Biological Sciences, Vanderbilt University, Nashville, TN, USA.
James P HeldDepartment of Biological Sciences, Vanderbilt University, Nashville, TN, USA.ORCID 0000-0003-4322-2108
David M McCandlishSimons Center for Quantitative Biology, Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, 11724, USA.ORCID 0009-0006-1474-0407
Maulik R PatelDepartment of Biological Sciences, Vanderbilt University, Nashville, TN, USA. maulik.r.patel@vanderbilt.edu.ORCID 0000-0003-3749-0122

Funding

TRAINING PROGRAM IN CELLULAR, BIOCHEMICAL, &MOLECULAR ST32GM008554 · NIGMS · VANDERBILT UNIVERSITY · PI PATTON, JAMES G. · 1995 to 2020
$7.4M
Computational analysis of complex genetic interactionsR35GM133613 · NIGMS · COLD SPRING HARBOR LABORATORY · PI David Martin McCandlish · 2019 to 2026
$3.5M
Mechanisms of mutant mitochondrial genome modulationR35GM145378 · NIGMS · VANDERBILT UNIVERSITY · PI MAULIK R PATEL · 2022 to 2026
$2.4M
Regulation of mitochondrial heteroplasmy dynamicsR01GM123260 · NIGMS · VANDERBILT UNIVERSITY · PI PATEL, MAULIK R · 2017 to 2021
$1.5M
Mechanisms underlying mutant mitochondrial genome dynamicsF31GM125344 · NIGMS · VANDERBILT UNIVERSITY · PI GITSCHLAG, BRYAN L. · 2017 to 2018
$57k
NIGMS NIH HHS F31 GM125344NIGMS NIH HHS R01 GM123260NIGMS NIH HHS R35 GM133613NIGMS NIH HHS R35 GM145378NIGMS NIH HHS T32 GM008554U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) F31GM125344U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) R01GM123260U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) R35GM133613U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) R35GM145378
6 · The paper itself

Abstract

Cells possess multiple mitochondrial DNA (mtDNA) copies, which undergo semi-autonomous replication and stochastic inheritance. This enables mutant mtDNA variants to arise and selfishly compete with cooperative (wildtype) mtDNA. Selfish mitochondrial genomes are subject to selection at different levels: they compete against wildtype mtDNA directly within hosts and indirectly through organism-level selection. However, determining the relative contributions of selection at different levels has proven challenging. We overcome this challenge by combining mathematical modeling with experiments designed to isolate the levels of selection. Applying this approach to many selfish mitochondrial genotypes in Caenorhabditis elegans reveals an unexpected diversity of evolutionary mechanisms. Some mutant genomes persist at high frequency for many generations, despite a host fitness cost, by aggressively outcompeting cooperative genomes within hosts. Conversely, some mutant genomes persist by evading inter-organismal selection. Strikingly, the mutant genomes vary dramatically in their susceptibility to genetic drift. Although different mechanisms can cause high frequency of selfish mtDNA, we show how they give rise to characteristically different distributions of mutant frequency among individuals. Given that heteroplasmic frequency represents a key determinant of phenotypic severity, this work outlines an evolutionary theoretic framework for predicting the distribution of phenotypic consequences among individuals carrying a selfish mitochondrial genome.

Indexed as

Caenorhabditis elegansDNA, MitochondrialEvolution, MolecularGenome, MitochondrialMutationAnimalsGenetic DriftGenotypeMitochondriaModels, GeneticSelection, GeneticDNA, Mitochondrial

Identifiers

PMID39300074
PMCPMC11413162

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.