Evidence map›Paper›PMID 39419865›Full record

ArticleMolecular biology reports2024

Identification of a novel alternate promoter element in the pheST operon of Escherichia coli.

Praveen Belagal

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In one paragraph

Article in Molecular biology reports, 2024. 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 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

2 citing papers in PubMed.

  1. Article
  2. Genetic and molecular studies of fitC4 and its suppressors fitA76* and fit95 in Escherichia coli.International microbiology : the official journal of the Spanish Society for Microbiology · 2025
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author.

Praveen BelagalDepartment of Molecular Biology, School of Biological Sciences, Madurai Kamaraj University, Madurai, 625 021, India. prabelagal@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEarlier work in this laboratory revealed that fitA was same as pheS as a recombinant clone, pSRJ5R1 harboring pheS

methodsPlasmid clones with promoter-mutations or -deletions were constructed by PCR-based cloning and their ability to complement fitA76 Ts mutant strains was checked. Chromosomal mutations were transferred into various genetic backgrounds via P1-transductions. Relative viability assays were performed to check the extent of complementation.

resultsClones harboring point mutations (PM-pheS) or deletion (PD1-pheS) of - 10 region of the putative promoter did not abolish complementation of the fitA76 Ts phenotype. Subsequently, a novel alternate promoter (AP) was discovered by downstream deletion clone (PD2-pheS) which failed to complement. Keeping PD1-pheS intact but mutating initiation codon of pheS (ATG→TTG) failed to complement. Complementation ability of novel alternate promoter is poor in HfrC strain background unlike native promoter which complements well independent of strain background.

conclusionA novel alternate-promoter of pheST operon was identified by mutational/deletional analyses and earlier reported putative - 10 promoter was shown to be dispensable. Alternate promoter is relA dependent.

Indexed as

Escherichia coliOperonPromoter Regions, GeneticBase SequenceEscherichia coli ProteinsGene Expression Regulation, BacterialGenetic Complementation TestMutationPlasmidsEscherichia coli ProteinsAlternate promoterEscherichia colifitfitA76PheRSpheST operon

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Registered trials

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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.