Evidence map›Paper›PMID 19542281›Full record

ArticleJournal of bacteriology2009

SlyA, a MarR family transcriptional regulator, is essential for virulence in Dickeya dadantii 3937.

M Manjurul Haque, M Shahinur Kabir, Luqman Qurata Aini, Hisae Hirata, Shinji Tsuyumu

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Journal of bacteriology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.2field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 65 citations in OpenAlex.

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  11. The MarR-Type Regulator PA3458 Is Involved in Osmoadaptation Control inInternational journal of molecular sciences · 2021
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

M Manjurul HaqueFaculty of Agriculture, Shizuoka University, Shizuoka, Japan. tsuyumu@agr.shizuoka.ac.jp.
M Shahinur Kabir
Luqman Qurata Aini
Hisae Hirata
Shinji Tsuyumu
Shizuoka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SlyA, a MarR family transcriptional regulator, controls an assortment of biological functions in several animal-pathogenic bacteria. In order to elucidate the functions of SlyA in the phytopathogen Dickeya dadantii (formerly Erwinia chrysanthemi) 3937, a slyA gene deletion mutant (denoted DeltaslyA) was constructed. The mutant exhibited increased sensitivity to sodium hypochlorite, the cationic antimicrobial peptide polymyxin B, and oxidative stress. The mutant showed reduced production of pectate lyase and exopolysaccharide and an inability to form a pellicle. The mutant lacking a functional slyA gene showed a significantly reduced ability to cause maceration of potato tubers. Accordingly, the mutant exhibited significantly reduced bacterial growth and failed to hyperinduce pectate lyase production in planta. Introduction of a plasmid containing slyA into the DeltaslyA mutant caused all of these phenotypes to recover to wild-type levels. These results suggest that SlyA plays an important role in virulence to plants by positively regulating the expression of multiple pathogenicity-related traits of D. dadantii 3937.

Indexed as

Anti-Bacterial AgentsBacterial ProteinsDickeya chrysanthemiGene DeletionOxidantsPlant DiseasesPlant RootsPolymyxin BPolysaccharide-LyasesPolysaccharides, BacterialSodium HypochloriteSolanum tuberosumTranscription FactorsVirulenceAnti-Bacterial AgentsBacterial ProteinsOxidantspectate lyasePolymyxin BPolysaccharide-LyasesPolysaccharides, BacterialSodium HypochloriteTranscription Factors

Identifiers

PMID19542281
PMCPMC2725626
OpenAlexW2005734816

What OpenQuestion holds

Textmetadata
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.