Evidence map›Paper›PMID 32868761›Full record

ArticleNature communications2020

Entropy of a bacterial stress response is a generalizable predictor for fitness and antibiotic sensitivity.

Zeyu Zhu, Defne Surujon, Juan C Ortiz-Marquez, Wenwen Huo, Ralph R Isberg, José Bento, Tim van Opijnen

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. 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
5.4field-weighted citation impact, top 4% 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, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

7 authors at 2 institutions in 1 country.

Zeyu Zhu *Biology Department, Boston College, Chestnut Hill, MA, 02467, USA.ORCID http://orcid.org/0000-0002-9218-9351
Defne Surujon *Biology Department, Boston College, Chestnut Hill, MA, 02467, USA.ORCID http://orcid.org/0000-0001-7964-3057
Juan C Ortiz-MarquezBiology Department, Boston College, Chestnut Hill, MA, 02467, USA.
Wenwen HuoDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, MA, 02111, USA.ORCID http://orcid.org/0000-0001-5112-1951
Ralph R IsbergDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, MA, 02111, USA.ORCID http://orcid.org/0000-0002-8330-3554
José BentoComputer Science Department, Boston College, Chestnut Hill, MA, 02467, USA.
Tim van OpijnenBiology Department, Boston College, Chestnut Hill, MA, 02467, USA. vanopijn@bc.edu.ORCID http://orcid.org/0000-0001-6895-6795
Boston College · USTufts University · 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
The bacterial response to antibiotics and the evolution of antibiotic resistanceR01AI110724 · NIAID · BOSTON COLLEGE · PI VAN OPIJNEN, TIM · 2015 to 2019
$2.0M
NIAID NIH HHS R01 AI110724NIAID NIH HHS U01 AI124302
6 · The paper itself

Abstract

Current approaches explore bacterial genes that change transcriptionally upon stress exposure as diagnostics to predict antibiotic sensitivity. However, transcriptional changes are often specific to a species or antibiotic, limiting implementation to known settings only. While a generalizable approach, predicting bacterial fitness independent of strain, species or type of stress, would eliminate such limitations, it is unclear whether a stress-response can be universally captured. By generating a multi-stress and species RNA-Seq and experimental evolution dataset, we highlight the strengths and limitations of existing gene-panel based methods. Subsequently, we build a generalizable method around the observation that global transcriptional disorder seems to be a common, low-fitness, stress response. We quantify this disorder using entropy, which is a specific measure of randomness, and find that in low fitness cases increasing entropy and transcriptional disorder results from a loss of regulatory gene-dependencies. Using entropy as a single feature, we show that fitness and quantitative antibiotic sensitivity predictions can be made that generalize well beyond training data. Furthermore, we validate entropy-based predictions in 7 species under antibiotic and non-antibiotic conditions. By demonstrating the feasibility of universal predictions of bacterial fitness, this work establishes the fundamentals for potentially new approaches in infectious disease diagnostics.

Indexed as

Directed Molecular EvolutionStress, PhysiologicalAnti-Bacterial AgentsBacteriaBacterial Physiological PhenomenaCommunicable DiseasesDrug Resistance, BacterialEntropyGene Expression Regulation, BacterialGenes, BacterialGenome, BacterialSequence Analysis, RNAStreptococcus pneumoniaeTranscriptomeAnti-Bacterial Agents

Identifiers

PMID32868761
PMCPMC7458919
OpenAlexW3082227610

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.