Evidence map›Paper›PMID 41099138›Full record

ArticleMolecular biology and evolution2025

Unraveling Epistatic Interactions Between Sites Under Drug-Dependent Selection in the Mycobacterium tuberculosis Genome.

Anfisa V Popova, Daria I Bykova, Gennady G Fedonin, Dmitry V Bosov, Kirill O Reshetnikov, Alexey D Neverov

Abstract read
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Article in Molecular biology and evolution, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Anfisa V PopovaInternational Laboratory of Statistical and Computational Genomics, HSE University, Moscow 109028, Russian Federation.ORCID 0000-0001-9365-7324
Daria I BykovaBioinformatics Research Group, Central Research Institute for Epidemiology, Moscow 111123, Russian Federation.ORCID 0009-0000-1224-0720
Gennady G FedoninBioinformatics Research Group, Central Research Institute for Epidemiology, Moscow 111123, Russian Federation.ORCID 0000-0002-9427-8083
Dmitry V BosovFaculty of Bioengineering and Bioinformatics, Lomonosov Moscow State University, Moscow 119991, Russian Federation.ORCID 0009-0004-0800-6682
Kirill O ReshetnikovBioinformatics Research Group, Central Research Institute for Epidemiology, Moscow 111123, Russian Federation.ORCID 0009-0003-9281-4238
Alexey D NeverovInternational Laboratory of Statistical and Computational Genomics, HSE University, Moscow 109028, Russian Federation.ORCID 0000-0002-3594-1682

Funding

Russian Science Foundation 25-21-00424
6 · The paper itself

Abstract

Many Mycobacterium tuberculosis genome sites experience different selective forces depending on whether a patient is treated with antibiotics. Here, we searched for pairs of such sites that evolve interdependently. We reconstructed the phylogeny of more than 11,000 Mycobacterium tuberculosis clinical isolates with known phenotypes for at least one of the 13 antitubercular drugs. By analyzing the distributions of substitutions and phenotypic state changes on the phylogeny, we identified sites where substitutions were associated with the acquisition of drug resistance or occurred preferentially in resistant or susceptible lineages. Among these sites, we searched for concordantly and discordantly evolving site pairs, carefully accounting for the presence of drug-associated selection and other coordinated selective forces. We identified one concordantly evolving site pair and 14 discordantly evolving site pairs between sites that are known to be strongly associated with resistance to antitubercular drugs. The concordantly evolving site pair and five out of 14 discordantly evolving site pairs were between sites whose substitutions were associated with resistance to different drugs, while the other nine discordantly evolving site pairs were between sites located either in the same genes or in different genes involved in alternative adaptive pathways to the same drugs. Overall, our findings emphasize the dual role of epistasis, which can both promote and limit the acquisition of resistance to multiple drugs.

Indexed as

Epistasis, GeneticGenome, BacterialMycobacterium tuberculosisAntitubercular AgentsDrug Resistance, BacterialEvolution, MolecularHumansPhylogenySelection, GeneticAntitubercular Agentsantibiotic resistanceepistasisfitness landscapeMycobacterium tuberculosis

Identifiers

PMID41099138
PMCPMC12632196

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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.