{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,12]],"date-time":"2025-10-12T04:40:37Z","timestamp":1760244037570,"version":"build-2065373602"},"reference-count":37,"publisher":"MDPI AG","issue":"21","license":[{"start":{"date-parts":[[2022,10,24]],"date-time":"2022-10-24T00:00:00Z","timestamp":1666569600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"the Skylark Food Science Institute"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Chromosome damage combined with defective recombinase activity renders cells inviable, owing to deficient double-strand break repair. Despite this, recA polA cells grow well under either DNA damage response (SOS) conditions or catalase medium supplementation. Catalase treatments reduce intracellular reactive oxygen species (ROS) levels, suggesting that recA polA cells are susceptible to not only chronic chromosome damage but also ROS. In this study, we used a reducing agent, vitamin C, to confirm whether cell growth could be improved. Vitamin C reduced ROS levels and rescued colony formation in recAts polA cells under restrictive temperatures in the presence of hslO, the gene encoding a redox molecular chaperone. Subsequently, we investigated the role of hslO in the cell growth failure of recAts polA cells. The effects of vitamin C were observed in hslO+ cells; simultaneously, cells converged along several ploidies likely through a completion of replication, with the addition of vitamin C at restrictive temperatures. These results suggest that HslO could manage oxidative stress to an acceptable level, allowing for cell division as well as rescuing cell growth. Overall, ROS may regulate several processes, from damage response to cell division. Our results provide a basis for understanding the unsolved regulatory interplay of cellular processes.<\/jats:p>","DOI":"10.3390\/ijms232112786","type":"journal-article","created":{"date-parts":[[2022,10,24]],"date-time":"2022-10-24T06:37:45Z","timestamp":1666593465000},"page":"12786","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Vitamin C Maintenance against Cell Growth Arrest and Reactive Oxygen Species Accumulation in the Presence of Redox Molecular Chaperone hslO Gene"],"prefix":"10.3390","volume":"23","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3404-6253","authenticated-orcid":false,"given":"Akihiro","family":"Kaidow","sequence":"first","affiliation":[{"name":"Department of Biology, School of Biological Sciences, Tokai University, Sapporo 005-8601, Japan"},{"name":"Hokkaido Regional Research Center, Tokai University, Sapporo 005-8601, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Noriko","family":"Ishii","sequence":"additional","affiliation":[{"name":"Department of Biology, School of Biological Sciences, Tokai University, Sapporo 005-8601, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shingo","family":"Suzuki","sequence":"additional","affiliation":[{"name":"Department of Molecular Life Science, School of Medicine, Tokai University, Isehara 259-1193, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2067-6708","authenticated-orcid":false,"given":"Takashi","family":"Shiina","sequence":"additional","affiliation":[{"name":"Department of Molecular Life Science, School of Medicine, Tokai University, Isehara 259-1193, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hirokazu","family":"Kasahara","sequence":"additional","affiliation":[{"name":"Department of Biology, School of Biological Sciences, Tokai University, Sapporo 005-8601, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2022,10,24]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"1483","DOI":"10.1093\/genetics\/139.4.1483","article-title":"The mechanism of recA polA Lethality: Suppression by RecA-independent recombination repair activated by the lexA(Def) mutation in Escherichia coli","volume":"139","author":"Cao","year":"1995","journal-title":"Genetics"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"396","DOI":"10.1007\/s00203-022-02957-z","article-title":"Reactive oxygen species accumulation is synchronised with growth inhibition of temperature-sensitive recAts polA Escherichia coli","volume":"204","author":"Kaidow","year":"2022","journal-title":"Arch. 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