Evidence map›Paper›PMID 19028900›Full record

ArticleJournal of bacteriology2009

Glucose- and glucokinase-controlled mal gene expression in Escherichia coli.

Christina Lengsfeld, Stefan Schönert, Renate Dippel, Winfried Boos

Open 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. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.7field-weighted citation impact, top 29% 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, 25 citations in OpenAlex.

  1. Article
  2. Characterizing lysine acetylation of glucokinase.Protein science : a publication of the Protein Society · 2024
    Article
  3. Article
  4. Review
  5. Secretome Analysis ofProteomes · 2021
    Article
  6. Article
  7. The interplay between effector binding and allostery in an engineered protein switch.Protein science : a publication of the Protein Society · 2016
    Article
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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

4 authors at 1 institution in 1 country.

Christina LengsfeldDepartment of Biology, University of Konstanz, 78457 Konstanz, Germany.
Stefan Schönert
Renate Dippel
Winfried Boos
University of Konstanz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MalT is the central transcriptional activator of all mal genes in Escherichia coli. Its activity is controlled by the inducer maltotriose. It can be inhibited by the interaction with certain proteins, and its expression can be controlled. We report here a novel aspect of mal gene regulation: the effect of cytoplasmic glucose and glucokinase (Glk) on the activity and the expression of MalT. Amylomaltase (MalQ) is essential for the metabolism of maltose. It forms maltodextrins and glucose from maltose or maltodextrins. We found that glucose above a concentration of 0.1 mM blocked the activity of the enzyme. malQ mutants when grown in the absence of maltodextrins are endogenously induced by maltotriose that is derived from the degradation of glycogen. Therefore, the fact that glk malQ(+) mutants showed elevated mal gene expression finds its explanation in the reduced ability to remove glucose from MalQ-catalyzed maltodextrin formation and is caused by a metabolically induced MalQ(-) phenotype. However, even in mutants lacking glycogen, Glk controls endogenous induction. We found that overexpressed Glk due to its structural similarity with Mlc, the repressor of malT, binds to the glucose transporter (PtsG), releasing Mlc and thus increasing malT repression. In addition, even in mutants lacking Mlc (and glycogen), the overexpression of glk leads to a reduction in mal gene expression. We interpret this repression by a direct interaction of Glk with MalT concomitant with MalT inhibition. This repression was dependent on the presence of either maltodextrin phosphorylase or amylomaltase and led to the inactivation of MalT.

Indexed as

Chromatography, Thin LayerEnzyme ActivationEscherichia coliEscherichia coli ProteinsGene Expression Regulation, BacterialGlucokinaseGlucoseGlucose Transport Proteins, FacilitativeGlycogen Debranching Enzyme SystemMutationProtein BindingTrisaccharides4 alpha-glucanotransferaseEscherichia coli ProteinsGlucokinaseGlucoseGlucose Transport Proteins, FacilitativeGlycogen Debranching Enzyme SystemmaltotrioseTrisaccharides

Identifiers

PMID19028900
PMCPMC2632087
OpenAlexW2139208071

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.