Evidence map›Paper›PMID 30666816›Full record

ArticleBiotechnology progress2019

Plasmid-encoded protein attenuates Escherichia coli swimming velocity and cell growth, not reprogrammed regulatory functions.

Chelsea Virgile, Pricila Hauk, Hsuan-Chen Wu, William E Bentley

Open access · greenAbstract read
In one paragraph

Article in Biotechnology progress, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. 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

4 authors at 2 institutions in 1 country.

Chelsea VirgileInstitute for Bioscience and Biotechnology Research, MD, 20742.
Pricila HaukInstitute for Bioscience and Biotechnology Research, MD, 20742.
Hsuan-Chen WuDept. of Biochemical Science and Technology, National Taiwan University, Taipei City, Taiwan.
William E BentleyInstitute for Bioscience and Biotechnology Research, MD, 20742.ORCID 0000-0002-4855-7866
Institute for Bioscience and Biotechnology ResearchNational Taiwan University · TW

Funding

Accessing molecular communication via synthetic biology and microelectronics – gut on a chip modelR21EB024102 · NIBIB · UNIV OF MARYLAND, COLLEGE PARK · PI BENTLEY, WILLIAM E. · 2017 to 2018
$412k
NIBIB NIH HHS R21 EB024102
6 · The paper itself

Abstract

In addition to engineering new pathways for synthesis, synthetic biologists rewire cells to carry out "programmable" functions, an example being the creation of wound-healing probiotics. Engineering regulatory circuits and synthetic machinery, however, can be deleterious to cell function, particularly if the "metabolic burden" is significant. Here, a synthetic regulatory circuit previously constructed to direct Escherichia coli to swim toward hydrogen peroxide, a signal of wound generation, was shown to work even with coexpression of antibiotic resistance genes and genes associated with lactose utilization. We found, however, that cotransformation with a second vector constitutively expressing GFP (as a marker) and additionally conferring resistance to kanamycin and tetracycline resulted in slower velocity (Δ~6 μm/s) and dramatically reduced growth rate (Δ > 50%). The additional vector did not, however, alter the run-and-tumble ratio or directional characteristics of H

Indexed as

Escherichia coliEscherichia coli ProteinsKineticsPlasmidsEscherichia coli ProteinsCheZconstitutive fluorescencemetabolic burdenmotilitysynthetic biology

Identifiers

PMID30666816
PMCPMC10711804
OpenAlexW2911455598

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.