Evidence map›Paper›PMID 16707676›Full record

ArticleJournal of bacteriology2006

The superoxide dismutases of Bacillus anthracis do not cooperatively protect against endogenous superoxide stress.

Karla D Passalacqua, Nicholas H Bergman, Amy Herring-Palmer, Philip Hanna

Open access · greenAbstract read
In one paragraph

Article in Journal of bacteriology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 51 citations in OpenAlex.

  1. Why is manganese so valuable to bacterial pathogens?Frontiers in cellular and infection microbiology · 2023
    Review
  2. Article
  3. Isocitrate dehydrogenase of Bacillus cereus is involved in biofilm formation.World journal of microbiology & biotechnology · 2021
    Article
  4. Article
  5. Roles of the Two-MnSOD System ofInternational journal of molecular sciences · 2019
    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.

Karla D PassalacquaDepartment of Microbiology and Immunology, University of Michigan Medical School, 1150 West Medical Center Drive, 6703 Medical Science Building II, Ann Arbor, MI 48109, USA.
Nicholas H Bergman
Amy Herring-Palmer
Philip Hanna
University of Michigan–Ann Arbor · US

Funding

Cellular Biotechnology Training Program (CBTP) - Years 31-35T32GM145304 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Guizhi Zhu · 2022 to 2026
$2.6M
IDENTIFYING TARGETS FOR THERAPEUTICS INTERVENTIONS USING PROTEOMICS TECHNOLOGYN01AI40059 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · 2007 to 2008
$1.1M
MACROPHAGE RESPONSES TO B. ANTHRACIS LETHAL TOXINF32AI008649 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI HANNA, PHILIP C · 1992 to 1995
–
NIAID NIH HHS AI 08649NIAID NIH HHS N01 AI040059NIAID NIH HHS N01 AI 40059NIGMS NIH HHS T32 GM145304
6 · The paper itself

Abstract

The Bacillus anthracis chromosome encodes four unique, putative superoxide dismutase (sod) genes. During exponential growth and sporulation, sodA1, sodA2, and sodC are transcribed constitutively throughout the growth cycle as individual genes. In contrast, the transcription of sod15 occurs mainly during late exponential and sporulation phases as part of a four-gene operon that may be involved in spore formation. Vegetative cell and spore lysates of wild-type Sterne and superoxide dismutase deletion (Deltasod) mutants show detectable SOD activity for SODA1 and SODA2, and protein analysis suggests that these two proteins form active homodimers and heterodimers. A comparison of the growth of parental versus Deltasod mutants under various chemical oxidative stresses indicates that DeltasodA1 mutants are particularly sensitive to endogenously produced superoxide, whereas DeltasodA2, Deltasod15, and DeltasodC mutants remain as resistant to this stress as the parental strain. In addition, in mouse survival assays, Deltasod15 and DeltasodA1 were responsible for less end-point death, but the level of decreased virulence does not fall within a statistically significant range. Collectively, these data show that sodA1 acts as a major protectant from intracellular superoxide stress, that sod15 is transcribed as part of an operon that may play a role in cell morphology, and that sodA2 and sodC may have minor roles that are not apparent in the conditions tested here.

Indexed as

Oxidative StressBacillus anthracisChromosome MappingFree Radical ScavengersGenome, BacterialIsoenzymesPlasmidsReverse Transcriptase Polymerase Chain ReactionSpores, BacterialSuperoxide DismutaseSuperoxidesFree Radical ScavengersIsoenzymesSuperoxide DismutaseSuperoxides

Identifiers

PMID16707676
PMCPMC1482891
OpenAlexW2146180738

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.