Evidence map›Paper›PMID 23363022›Full record

ArticleACS chemical biology2013

Directed evolution of the quorum-sensing regulator EsaR for increased signal sensitivity.

Jasmine Shong, Yao-Ming Huang, Christopher Bystroff, Cynthia H Collins

Open access · greenAbstract read
In one paragraph

Article in ACS chemical biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. Article
  3. Developing Quorum Sensing-Based Collaborative Dynamic Control System in Halomonas TD01.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Can the natural diversity of quorum-sensing advance synthetic biology?Frontiers in bioengineering and biotechnology · 2015
    Review
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

4 authors at 1 institution in 1 country.

Jasmine ShongDepartment of Chemical and Biological Engineering, Rensselaer Polytechnic Institute, 110 8th St., Troy, NY 12180, USA.
Yao-Ming Huang
Christopher Bystroff
Cynthia H Collins
Rensselaer Polytechnic Institute · US

Funding

Computational design of specific binding proteins using Leave-One-OutR01GM099827 · NIGMS · RENSSELAER POLYTECHNIC INSTITUTE · PI BONDOS, SARAH E, BYSTROFF, CHRISTOPHER · 2012 to 2021
$2.9M
Computational design of specific binding proteins using Leave-One-OutR21GM088838 · NIGMS · RENSSELAER POLYTECHNIC INSTITUTE · PI BYSTROFF, CHRISTOPHER · 2009 to 2010
$397k
NIGMS NIH HHS R01 GM099827NIGMS NIH HHS R21 GM088838
6 · The paper itself

Abstract

The use of cell-cell communication or "quorum sensing (QS)" elements from Gram-negative Proteobacteria has enabled synthetic biologists to begin engineering systems composed of multiple interacting organisms. However, additional tools are necessary if we are to progress toward synthetic microbial consortia that exhibit more complex, dynamic behaviors. EsaR from Pantoea stewartii subsp. stewartii is a QS regulator that binds to DNA as an apoprotein and releases the DNA when it binds to its cognate signal molecule, 3-oxohexanoyl-homoserine lactone (3OC6HSL). In the absence of 3OC6HSL, EsaR binds to DNA and can act as either an activator or a repressor of transcription. Gene expression from P(esaR), which is repressed by wild-type EsaR, requires 100- to 1000-fold higher concentrations of signal than commonly used QS activators, such as LuxR and LasR. Here we have identified EsaR variants with increased sensitivity to 3OC6HSL using directed evolution and a dual ON/OFF screening strategy. Although we targeted EsaR-dependent derepression of P(esaR), our EsaR variants also showed increased 3OC6HSL sensitivity at a second promoter, P(esaS), which is activated by EsaR in the absence of 3OC6HSL. Here, the increase in AHL sensitivity led to gene expression being turned off at lower concentrations of 3OC6HSL. Overall, we have increased the signal sensitivity of EsaR more than 70-fold and generated a set of EsaR variants that recognize 3OC6HSL concentrations ranging over 4 orders of magnitude. QS-dependent transcriptional regulators that bind to DNA and are active in the absence of a QS signal represent a new set of tools for engineering cell-cell communication-dependent gene expression.

Indexed as

Directed Molecular EvolutionQuorum SensingBacterial ProteinsModels, MolecularMutagenesis, Site-DirectedPantoeaRecombination, GeneticTranscription FactorsBacterial ProteinsEsaR protein, Pantoea stewartiiTranscription Factors

Identifiers

PMID23363022
PMCPMC4478592
OpenAlexW2318810578

What OpenQuestion holds

Textmetadata
LicenceTDM
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.