Evidence map›Paper›PMID 21613982›Full record

ArticleMolecular systems biology2011

Adaptation by stochastic switching of a monostable genetic circuit in Escherichia coli.

Saburo Tsuru, Nao Yasuda, Yoshie Murakami, Junya Ushioda, Akiko Kashiwagi, Shingo Suzuki, Kotaro Mori, Bei-Wen Ying, Tetsuya Yomo

Open access · goldAbstract read
In one paragraph

Article in Molecular systems biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

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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

9 authors at 3 institutions in 1 country.

Saburo TsuruDepartment of Bioinformatic Engineering, Graduate School of Information Science and Technology, Osaka University, Osaka, Japan.
Nao Yasuda
Yoshie Murakami
Junya Ushioda
Akiko Kashiwagi
Shingo Suzuki
Kotaro Mori
Bei-Wen Ying
Tetsuya Yomo
Osaka University · JPUbe Frontier University · JPHirosaki University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stochastic switching is considered as a cost-saving strategy for adaptation to environmental challenges. We show here that stochastic switching of a monostable circuit can mediate the adaptation of the engineered OSU12-hisC Escherichia coli strain to histidine starvation. In this strain, the hisC gene was deleted from the His operon and placed under the control of a monostable foreign promoter. In response to histidine depletion, the OSU12-hisC population shifted to a higher HisC expression level, which is beneficial under starving conditions but is not favoured by the monostable circuit. The population shift was accompanied by growth recovery and was reversible upon histidine addition. A weak directionality in stochastic switching of hisC was observed in growing microcolonies under histidine-free conditions. Directionality and fate decision were in part dependent on the initial cellular status. Finally, microarray analysis indicated that OSU12-hisC reorganized its transcriptome to reach the appropriate physiological state upon starvation. These findings suggest that bacteria do not necessarily need to evolve signalling mechanisms to control gene expression appropriately, even for essential genes.

Indexed as

Genes, BacterialAdaptation, PhysiologicalCloning, MolecularEscherichia coliGene DeletionGene Expression ProfilingGene Expression Regulation, BacterialHistidineOperonOrganisms, Genetically ModifiedHistidine

Identifiers

PMID21613982
PMCPMC3130557
OpenAlexW2079892401

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.