Evidence map›Paper›PMID 19820090›Full record

ArticleJournal of bacteriology2009

Growth phase and (p)ppGpp control of IraD, a regulator of RpoS stability, in Escherichia coli.

Houra Merrikh, Alexander E Ferrazzoli, Susan T Lovett

Open access · bronzeAbstract 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 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

36 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Broad-spectrum tolerance to disinfectant-mediated bacterial killing due to mutation of the PheS aminoacyl tRNA synthetase.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Review
  5. RpoS and the bacterial general stress response.Microbiology and molecular biology reviews : MMBR · 2024
    Review
  6. Article
  7. Review
  8. A negative feedback loop is critical for recovery of RpoS after stress inbioRxiv : the preprint server for biology · 2023
    Article
  9. Article
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  11. Article
  12. Review
  13. Review
  14. 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

3 authors at 1 institution in 1 country.

Houra MerrikhDepartment of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts 02454-9110, USA.
Alexander E Ferrazzoli
Susan T Lovett
Brandeis University · US

Funding

Replication Fork RepairR01GM051753 · NIGMS · BRANDEIS UNIVERSITY · PI LOVETT, SUSAN THOMAS · 1994 to 2025
$10.7M
GENETIC AND BIOCHEMICAL MECHANISMS OF REGULATIONT32GM007122 · NIGMS · BRANDEIS UNIVERSITY · PI LOVETT, SUSAN THOMAS · 1985 to 2020
$7.5M
NIGMS NIH HHS GM051753NIGMS NIH HHS R01 GM051753NIGMS NIH HHS T32 GM007122
6 · The paper itself

Abstract

The antiadaptor protein IraD inhibits the proteolysis of the alternative sigma factor, RpoS, which promotes the synthesis of >100 genes during the general stress response and during stationary phase. Our previous results showed that IraD determines RpoS steady-state levels during exponential growth and mediates its stabilization after DNA damage. In this study, we show by promoter fusions that iraD was upregulated during the transition from exponential growth to stationary phase. The levels of RpoS likewise rose during this transition in a partially IraD-dependent manner. The expression of iraD was under the control of ppGpp. The expression of iraD required RelA and SpoT (p)ppGpp synthetase activities and was dramatically induced by a "stringent" allele of RNA polymerase, culminating in elevated levels of RpoS. Surprisingly, DksA, normally required for transcriptional effects of the stringent response, repressed iraD expression, suggesting that DksA can exert regulatory effects independent of and opposing those of (p)ppGpp. Northern blot analysis and 5' rapid amplification of cDNA ends revealed two transcripts for iraD in wild-type strains; the smaller was regulated positively by RelA during growth; the larger transcript was induced specifically upon transition to stationary phase and was RelA SpoT dependent. A reporter fusion to the distal promoter indicated that it accounts for growth-phase regulation and DNA damage inducibility. DNA damage inducibility occurred in strains unable to synthesize (p)ppGpp, indicating an additional mode of regulation. Our results suggest that the induction of RpoS during transition to stationary phase and by (p)ppGpp occurs at least partially through IraD.

Indexed as

Cell CycleGene Expression Regulation, BacterialArtificial Gene FusionBacterial ProteinsBlotting, NorthernEscherichia coliEscherichia coli ProteinsGene Expression ProfilingGenes, ReporterGuanosine PentaphosphatePyrophosphatasesSigma FactorTranscription Factor RelABacterial ProteinsEscherichia coli Proteinsguanosine-3',5'-bis(diphosphate) 3'-pyrophosphataseGuanosine PentaphosphateIraD protein, E coliPyrophosphatasesSigma Factorsigma factor KatF protein, BacteriaTranscription Factor RelA

Identifiers

PMID19820090
PMCPMC2786607
OpenAlexW2011958733

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.