Evidence map›Paper›PMID 11466271›Full record

ArticleJournal of bacteriology2001

Requirement of novel competence genes pilT and pilU of Pseudomonas stutzeri for natural transformation and suppression of pilT deficiency by a hexahistidine tag on the type IV pilus protein PilAI.

S Graupner, N Weger, M Sohni, W Wackernagel

Abstract read
In one paragraph

Article in Journal of bacteriology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Article
  2. Comparative genomics ofFrontiers in microbiology · 2023
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. DNA Uptake by Type IV Filaments.Frontiers in molecular biosciences · 2019
    Review
  8. Uptake of extracellular DNA: competence induced pili in natural transformation of Streptococcus pneumoniae.BioEssays : news and reviews in molecular, cellular and developmental biology · 2015
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Biology of Pseudomonas stutzeri.Microbiology and molecular biology reviews : MMBR · 2006
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

4 authors.

S GraupnerGenetik, Fachbereich Biologie, Carl von Ossietzky Universität Oldenburg, D-26111 Oldenburg, Germany.
N Weger
M Sohni
W Wackernagel

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ubiquitous species Pseudomonas stutzeri has type IV pili, and these are essential for the natural transformation of the cells. An absolute transformation-deficient mutant obtained after transposon mutagenesis had an insertion in a gene which was termed pilT. The deduced amino acid sequence has identity with PilT of Pseudomonas aeruginosa (94%), Neisseria gonorrhoeae (67%), and other gram-negative species and it contains a nucleotide-binding motif. The mutant was hyperpiliated but defective for further pilus-associated properties, such as twitching motility and plating of pilus-specific phage PO4. [(3)H]thymidine-labeled DNA was bound by the mutant but not taken up. Downstream of pilT a gene, termed pilU, coding for a putative protein with 88% amino acid identity with PilU of P. aeruginosa was identified. Insertional inactivation did not affect piliation, twitching motility, or PO4 infection but reduced transformation to about 10%. The defect was fully complemented by PilU of nontransformable P. aeruginosa. When the pilAI gene (coding for the type IV pilus prepilin) was manipulated to code for a protein in which the six C-terminal amino acids were replaced by six histidine residues and then expressed from a plasmid, it gave a nonpiliated and twitching motility-defective phenotype in pilAI::Gm(r) cells but allowed transformability. Moreover, the mutant allele suppressed the absolute transformation deficiency caused by the pilT mutation. Considering the hypothesized role of pilT(+) in pilus retraction and the presumed requirement of retraction for DNA uptake, it is proposed that the pilT-independent transformation is promoted by PilA mutant protein either as single molecules or as minimal pilin assembly structures in the periplasm which may resemble depolymerized pili and that these cause the outer membrane pores to open for DNA entry.

Indexed as

Adenosine TriphosphatasesFimbriae ProteinsMolecular Motor ProteinsTransformation, BacterialBacterial Outer Membrane ProteinsBacterial ProteinsChromosomes, BacterialDNA, BacterialEscherichia coliFimbriae, BacterialGenetic Complementation TestGenotypeMutagenesis, InsertionalPlasmidsPseudomonasRestriction MappingAdenosine TriphosphatasesBacterial Outer Membrane ProteinsBacterial ProteinsDNA, BacterialFimbriae ProteinsMolecular Motor ProteinsPilU protein, Pseudomonas aeruginosa

Identifiers

PMID11466271
PMCPMC99522

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.