Evidence map›Paper›PMID 22544236›Full record

ArticleApplied and environmental microbiology2012

Involvement of Clostridium botulinum ATCC 3502 sigma factor K in early-stage sporulation.

David G Kirk, Elias Dahlsten, Zhen Zhang, Hannu Korkeala, Miia Lindström

Abstract read
In one paragraph

Article in Applied and environmental microbiology, 2012. 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

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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

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3 · Its place in the literature

Who cites it

22 citing papers in PubMed.

  1. Expression profiles of sporulation genes in multidrug-resistantExperimental biology and medicine (Maywood, N.J.) · 2023
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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

5 authors.

David G KirkDepartment of Food Hygiene and Environmental Health, Centre of Excellence in Microbial Food Safety Research, Faculty of Veterinary Medicine, University of Helsinki, Finland.
Elias Dahlsten
Zhen Zhang
Hannu Korkeala
Miia Lindström

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A key survival mechanism of Clostridium botulinum, the notorious neurotoxic food pathogen, is the ability to form heat-resistant spores. While the genetic mechanisms of sporulation are well understood in the model organism Bacillus subtilis, nothing is known about these mechanisms in C. botulinum. Using the ClosTron gene-knockout tool, sigK, encoding late-stage (stage IV) sporulation sigma factor K in B. subtilis, was disrupted in C. botulinum ATCC 3502 to produce two different mutants with distinct insertion sites and orientations. Both mutants were unable to form spores, and their elongated cell morphology suggested that the sporulation pathway was blocked at an early stage. In contrast, sigK-complemented mutants sporulated successfully. Quantitative real-time PCR analysis of sigK in the parent strain revealed expression at the late log growth phase in the parent strain. Analysis of spo0A, encoding the sporulation master switch, in the sigK mutant and the parent showed significantly reduced relative levels of spo0A expression in the sigK mutant compared to the parent strain. Similarly, sigF showed significantly lower relative transcription levels in the sigK mutant than the parent strain, suggesting that the sporulation pathway was blocked in the sigK mutant at an early stage. We conclude that σ(K) is essential for early-stage sporulation in C. botulinum ATCC 3502, rather than being involved in late-stage sporulation, as reported for the sporulation model organism B. subtilis. Understanding the sporulation mechanism of C. botulinum provides keys to control the public health risks that the spores of this dangerous pathogen cause through foods.

Indexed as

Gene Expression Regulation, BacterialClostridium botulinumGene Expression ProfilingGene Knockout TechniquesGenetic Complementation TestReal-Time Polymerase Chain ReactionSpores, BacterialTranscription Factorssigma KTranscription Factors

Identifiers

PMID22544236
PMCPMC3370484

What OpenQuestion holds

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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.