Evidence map›Paper›PMID 36564489›Full record

ArticleScientific reports2022

HslO ameliorates arrested ΔrecA polA cell growth and reduces DNA damage and oxidative stress responses.

A Kaidow, N Ishii, S Suzuki, T Shiina, K Endoh, Y Murakami, H Kasahara

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. The roles of theJournal of bacteriology · 2026
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  3. Genome-wide Screening of the Escherichia coli Keio Knockout Collection Identifies Genetic Determinants of Epetraborole Hypersusceptibility.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2025
    Article
  4. Article
  5. 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

7 authors at 1 institution in 1 country.

A KaidowDepartment of Biology, School of Biological Sciences, Tokai University, Sapporo, 005-8601, Japan. akaidow@tsc.u-tokai.ac.jp.
N IshiiDepartment of Biology, School of Biological Sciences, Tokai University, Sapporo, 005-8601, Japan.
S SuzukiDepartment of Molecular Medicine, School of Medicine, Tokai University, Isehara, 259-1193, Japan.
T ShiinaDepartment of Molecular Medicine, School of Medicine, Tokai University, Isehara, 259-1193, Japan.
K EndohDepartment of Biology, School of Biological Sciences, Tokai University, Sapporo, 005-8601, Japan.
Y MurakamiDepartment of Biology, School of Biological Sciences, Tokai University, Sapporo, 005-8601, Japan.
H KasaharaDepartment of Biology, School of Biological Sciences, Tokai University, Sapporo, 005-8601, Japan.
Tokai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromosome damage combined with defective recombinase activity has been widely considered to render cells inviable, owing to deficient double-strand break repair. However, temperature-sensitive recAts polA cells grow well upon induction of DNA damage and supplementation with catalase at restrictive temperatures. These treatments reduce intracellular reactive oxygen species (ROS) levels, which suggests that recAts polA cells are susceptible to ROS, but not chronic chromosome damage. Therefore, we investigated whether polA cells can tolerate a complete lack of recombinase function. We introduced a ΔrecA allele in polA cells in the presence or absence of the hslO-encoding redox molecular chaperon Hsp33 expression plasmid. Induction of the hslO gene with IPTG resulted in increased cell viability in ΔrecA polA cells with the hslO expression plasmid. ΔrecA polA cells in the absence of the hslO expression plasmid showed rich medium sensitivity with increasing ROS levels. Adding catalase to the culture medium considerably rescued growth arrest and decreased ROS. These results suggest that hslO expression manages oxidative stress to an acceptable level in cells with oxidative damage and rescues cell growth. Overall, ROS may regulate several processes, from damage response to cell division, via ROS-sensitive cell metabolism.

Indexed as

DNA DamageOxidative StressCatalaseReactive Oxygen SpeciesRecombinasesCatalaseReactive Oxygen SpeciesRecombinases

Identifiers

PMID36564489
PMCPMC9789031
OpenAlexW4312181073

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.