Evidence map›Paper›PMID 35672367›Full record

ArticleNature communications2022

A genome-wide atlas of antibiotic susceptibility targets and pathways to tolerance.

Dmitry Leshchiner, Federico Rosconi, Bharathi Sundaresh, Emily Rudmann, Luisa Maria Nieto Ramirez, Andrew T Nishimoto, Stephen J Wood, Bimal Jana, Noemí Buján, Kaicheng Li and 7 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.6field-weighted citation impact, top 8% of its field
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

27 citing papers in PubMed, 40 citations in OpenAlex.

  1. Widespread antibiotic-resistantOne health (Amsterdam, Netherlands) · 2026
    Article
  2. The phenotypic landscape of the model firmicuteProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
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  5. Regulation of PBP2x Surface Localization byPathogens (Basel, Switzerland) · 2026
    Article
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  10. Frontiers in bioinformatics · 2026
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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

17 authors at 2 institutions in 1 country.

Dmitry Leshchiner *Biology Department, Boston College, Chestnut Hill, MA, 02467, USA.
Federico Rosconi *Biology Department, Boston College, Chestnut Hill, MA, 02467, USA.ORCID 0000-0001-6760-9003
Bharathi Sundaresh *Biology Department, Boston College, Chestnut Hill, MA, 02467, USA.ORCID 0000-0002-1924-6612
Emily Rudmann *Biology Department, Boston College, Chestnut Hill, MA, 02467, USA.
Luisa Maria Nieto Ramirez *Biology Department, Boston College, Chestnut Hill, MA, 02467, USA.ORCID 0000-0003-1566-5876
Andrew T NishimotoDepartment of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.ORCID 0000-0003-1244-4656
Stephen J WoodBiology Department, Boston College, Chestnut Hill, MA, 02467, USA.ORCID 0000-0002-1306-1027
Bimal JanaBiology Department, Boston College, Chestnut Hill, MA, 02467, USA.
Noemí BujánBiology Department, Boston College, Chestnut Hill, MA, 02467, USA.ORCID 0000-0002-5353-8061
Kaicheng LiChemistry Department, Boston College, Chestnut Hill, MA, 02467, USA.
Jianmin GaoChemistry Department, Boston College, Chestnut Hill, MA, 02467, USA.ORCID 0000-0001-9341-1287
Matthew FrankDepartment of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.
Stephanie M ReeveDepartment of Chemical Biology and Therapeutics, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.ORCID 0000-0003-2064-405X
Richard E LeeDepartment of Chemical Biology and Therapeutics, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.ORCID 0000-0002-2397-0443
Charles O RockDepartment of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.ORCID 0000-0001-8648-4189
Jason W RoschDepartment of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.ORCID 0000-0002-1798-1760
Tim van OpijnenBiology Department, Boston College, Chestnut Hill, MA, 02467, USA. vanopijn@bc.edu.ORCID 0000-0001-6895-6795
Boston College · USSt. Jude Children's Research Hospital · US

Funding

Predicting the emergence of antibiotic resistance through multi-omics approaches and Immune System-surveillanU01AI124302 · NIAID · BOSTON COLLEGE · PI BENTO, JOSE, COOPER, VAUGHN · 2016 to 2020
$10.2M
REGULATION OF LIPID METABOLISM IN E COLIR01GM034496 · NIGMS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI ROCK, CHARLES O · 1985 to 2022
$9.2M
A priori adaptive evolution predictions for antibiotic resistance through genome-wide network analyses and machine learningR01AI148470 · NIAID · BOSTON COLLEGE · PI ORTIZ-MARQUEZ, JUAN CESAR FEDERICO, VAN OPIJNEN, TIM · 2020 to 2024
$2.0M
The bacterial response to antibiotics and the evolution of antibiotic resistanceR01AI110724 · NIAID · BOSTON COLLEGE · PI VAN OPIJNEN, TIM · 2015 to 2019
$2.0M
Novel Phage Display Platforms to Overcome Colistin ResistanceR01GM124231 · NIGMS · BOSTON COLLEGE · PI GAO, JIANMIN · 2019 to 2022
$1.2M
NIAID NIH HHS R01 AI110724NIAID NIH HHS R01 AI148470NIAID NIH HHS U01 AI124302NIGMS NIH HHS R01 GM034496NIGMS NIH HHS R01 GM124231
6 · The paper itself

Abstract

Detailed knowledge on how bacteria evade antibiotics and eventually develop resistance could open avenues for novel therapeutics and diagnostics. It is thereby key to develop a comprehensive genome-wide understanding of how bacteria process antibiotic stress, and how modulation of the involved processes affects their ability to overcome said stress. Here we undertake a comprehensive genetic analysis of how the human pathogen Streptococcus pneumoniae responds to 20 antibiotics. We build a genome-wide atlas of drug susceptibility determinants and generated a genetic interaction network that connects cellular processes and genes of unknown function, which we show can be used as therapeutic targets. Pathway analysis reveals a genome-wide atlas of cellular processes that can make a bacterium less susceptible, and often tolerant, in an antibiotic specific manner. Importantly, modulation of these processes confers fitness benefits during active infections under antibiotic selection. Moreover, screening of sequenced clinical isolates demonstrates that mutations in genes that decrease antibiotic sensitivity and increase tolerance readily evolve and are frequently associated with resistant strains, indicating such mutations could be harbingers for the emergence of antibiotic resistance.

Indexed as

Anti-Bacterial AgentsStreptococcus pneumoniaeDrug Resistance, MicrobialDrug ToleranceHumansMicrobial Sensitivity TestsAnti-Bacterial Agents

Identifiers

PMID35672367
PMCPMC9174251
OpenAlexW4281654286

What OpenQuestion holds

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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.