Evidence map›Paper›PMID 27162347›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Type IV pilins regulate their own expression via direct intramembrane interactions with the sensor kinase PilS.

Sara L N Kilmury, Lori L Burrows

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

43 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
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  4. Review
  5. Article
  6. Type IV pilin regulation: a transcriptional overview.Critical reviews in microbiology · 2026
    Review
  7. Separation ofmBio · 2025
    Article
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  12. Review
  13. Nutrient Limitation SensitizesACS infectious diseases · 2023
    Article
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  19. Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  20. Article
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

2 authors at 1 institution in 1 country.

Sara L N KilmuryDepartment of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON, Canada L8S 4K1; Michael G. DeGroote Institute for Infectious Diseases Research, McMaster University, Hamilton, ON, Canada L8S 4K1.
Lori L BurrowsDepartment of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON, Canada L8S 4K1; Michael G. DeGroote Institute for Infectious Diseases Research, McMaster University, Hamilton, ON, Canada L8S 4K1 burrowl@mcmaster.ca.ORCID 0000-0003-0838-5040
McMaster University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type IV pili are important virulence factors for many pathogens, including Pseudomonas aeruginosa Transcription of the major pilin gene-pilA-is controlled by the PilS-PilR two-component system in response to unknown signals. The absence of a periplasmic sensing domain suggested that PilS may sense an intramembrane signal, possibly PilA. We suggest that direct interactions between PilA and PilS in the inner membrane reduce pilA transcription when PilA levels are high. Overexpression in trans of PilA proteins with diverse and/or truncated C termini decreased native pilA transcription, suggesting that the highly conserved N terminus of PilA was the regulatory signal. Point mutations in PilA or PilS that disrupted their interaction prevented autoregulation of pilA transcription. A subset of PilA point mutants retained the ability to interact with PilS but could no longer decrease pilA transcription, suggesting that interaction between the pilin and sensor kinase is necessary but not sufficient for pilA autoregulation. Furthermore, PilS's phosphatase motif was required for the autoregulation of pilA transcription, suggesting that under conditions where PilA is abundant, the PilA-PilS interaction promotes PilR dephosphorylation and thus down-regulation of further pilA transcription. These data reveal a clever bacterial inventory control strategy in which the major subunit of an important P. aeruginosa virulence factor controls its own expression.

Indexed as

Bacterial ProteinsFimbriae ProteinsGene Expression Regulation, BacterialMutationPhosphorylationPromoter Regions, GeneticPseudomonas aeruginosaTranscription FactorsTranscription, GeneticBacterial ProteinsFimbriae ProteinspilS protein, BacteriaTranscription FactorsGeobacter sulfurreducensPseudomonas aeruginosatranscriptional regulationtwo-component systemtype IV pili

Identifiers

PMID27162347
PMCPMC4889343
OpenAlexW2374649359

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.