Evidence map›Paper›PMID 24914186›Full record

ArticleJournal of bacteriology2014

Error-prone processing of apurinic/apyrimidinic (AP) sites by PolX underlies a novel mechanism that promotes adaptive mutagenesis in Bacillus subtilis.

Rocío del Carmen Barajas-Ornelas, Fernando H Ramírez-Guadiana, Rafael Juárez-Godínez, Victor M Ayala-García, Eduardo A Robleto, Ronald E Yasbin, Mario Pedraza-Reyes

Open access · bronzeAbstract read
In one paragraph

Article in Journal of bacteriology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 26 citations in OpenAlex.

  1. Germination and Outgrowth ofMicroorganisms · 2025
    Article
  2. Microbiology and molecular biology reviews : MMBR · 2024
    Review
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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

7 authors at 3 institutions in 2 countries.

Rocío del Carmen Barajas-OrnelasDepartment of Biology, Division of Natural and Exact Sciences, University of Guanajuato, Guanajuato, Mexico.
Fernando H Ramírez-GuadianaDepartment of Biology, Division of Natural and Exact Sciences, University of Guanajuato, Guanajuato, Mexico.
Rafael Juárez-GodínezDepartment of Biology, Division of Natural and Exact Sciences, University of Guanajuato, Guanajuato, Mexico.
Victor M Ayala-GarcíaDepartment of Biology, Division of Natural and Exact Sciences, University of Guanajuato, Guanajuato, Mexico.
Eduardo A RobletoSchool of Life Sciences, University of Nevada, Las Vegas, Nevada, USA.
Ronald E YasbinCollege of Arts and Sciences, University of Missouri-St. Louis, St. Louis, Missouri, USA.
Mario Pedraza-ReyesDepartment of Biology, Division of Natural and Exact Sciences, University of Guanajuato, Guanajuato, Mexico pedrama@ugto.mx.
Universidad de Guanajuato · MXUniversity of Missouri–St. Louis · USUniversity of Nevada, Las Vegas · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In growing cells, apurinic/apyrimidinic (AP) sites generated spontaneously or resulting from the enzymatic elimination of oxidized bases must be processed by AP endonucleases before they compromise cell integrity. Here, we investigated how AP sites and the processing of these noncoding lesions by the AP endonucleases Nfo, ExoA, and Nth contribute to the production of mutations (hisC952, metB5, and leuC427) in starved cells of the Bacillus subtilis YB955 strain. Interestingly, cells from this strain that were deficient for Nfo, ExoA, and Nth accumulated a greater amount of AP sites in the stationary phase than during exponential growth. Moreover, under growth-limiting conditions, the triple nfo exoA nth knockout strain significantly increased the amounts of adaptive his, met, and leu revertants produced by the B. subtilis YB955 parental strain. Of note, the number of stationary-phase-associated reversions in the his, met, and leu alleles produced by the nfo exoA nth strain was significantly decreased following disruption of polX. In contrast, during growth, the reversion rates in the three alleles tested were significantly increased in cells of the nfo exoA nth knockout strain deficient for polymerase X (PolX). Therefore, we postulate that adaptive mutations in B. subtilis can be generated through a novel mechanism mediated by error-prone processing of AP sites accumulated in the stationary phase by the PolX DNA polymerase.

Indexed as

Adaptation, BiologicalDNA DamageDNA RepairBacillus subtilisDNA-(Apurinic or Apyrimidinic Site) LyaseDNA-Directed DNA PolymeraseDNA Repair EnzymesMutationDNA-(Apurinic or Apyrimidinic Site) LyaseDNA-Directed DNA PolymeraseDNA polymerase XDNA Repair Enzymes

Identifiers

PMID24914186
PMCPMC4135629
OpenAlexW1997360220

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.