{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T21:04:30Z","timestamp":1761599070646},"reference-count":43,"publisher":"American Society for Microbiology","issue":"21","license":[{"start":{"date-parts":[[2006,11,1]],"date-time":"2006-11-01T00:00:00Z","timestamp":1162339200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Bacteriol"],"published-print":{"date-parts":[[2006,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:italic>Escherichia coli<\/jats:italic>\n            cells with mutations in\n            <jats:italic>recBC<\/jats:italic>\n            genes are defective for the main RecBCD pathway of recombination and have severe reductions in conjugational and transductional recombination, as well as in recombinational repair of double-stranded DNA breaks. This phenotype can be corrected by suppressor mutations in\n            <jats:italic>sbcB<\/jats:italic>\n            and\n            <jats:italic>sbcC<\/jats:italic>\n            (\n            <jats:italic>D<\/jats:italic>\n            ) genes, which activate an alternative RecF pathway of recombination. It was previously suggested that\n            <jats:italic>sbcB15<\/jats:italic>\n            and \u0394\n            <jats:italic>sbcB<\/jats:italic>\n            mutations, both of which inactivate exonuclease I, are equally efficient in suppressing the\n            <jats:italic>recBC<\/jats:italic>\n            phenotype. In the present work we reexamined the effects of\n            <jats:italic>sbcB15<\/jats:italic>\n            and \u0394\n            <jats:italic>sbcB<\/jats:italic>\n            mutations on DNA repair after UV and \u03b3 irradiation, on conjugational recombination, and on the viability of\n            <jats:italic>recBC<\/jats:italic>\n            (\n            <jats:italic>sbcC<\/jats:italic>\n            ) cells. We found that the\n            <jats:italic>sbcB15<\/jats:italic>\n            mutation is a stronger\n            <jats:italic>recBC<\/jats:italic>\n            suppressor than \u0394\n            <jats:italic>sbcB<\/jats:italic>\n            , suggesting that some unspecified activity of the mutant SbcB15 protein may be favorable for recombination in the RecF pathway. We also showed that the\n            <jats:italic>xonA2<\/jats:italic>\n            mutation, a member of another class of ExoI mutations, had the same effect on recombination as \u0394\n            <jats:italic>sbcB<\/jats:italic>\n            , suggesting that it is an\n            <jats:italic>sbcB<\/jats:italic>\n            null mutation. In addition, we demonstrated that recombination in a\n            <jats:italic>recBC sbcB15 sbcC<\/jats:italic>\n            mutant is less affected by\n            <jats:italic>recF<\/jats:italic>\n            and\n            <jats:italic>recQ<\/jats:italic>\n            mutations than recombination in\n            <jats:italic>recBC<\/jats:italic>\n            \u0394\n            <jats:italic>sbcB sbcC<\/jats:italic>\n            and\n            <jats:italic>recBC xonA2 sbcC<\/jats:italic>\n            strains is, indicating that SbcB15 alleviates the requirement for the RecFOR complex and RecQ helicase in recombination processes. Our results suggest that two types of\n            <jats:italic>sbcB<\/jats:italic>\n            -sensitive RecF pathways can be distinguished in\n            <jats:italic>E. coli<\/jats:italic>\n            , one that is activated by the\n            <jats:italic>sbcB15<\/jats:italic>\n            mutation and one that is activated by\n            <jats:italic>sbcB<\/jats:italic>\n            null mutations. Possible roles of SbcB15 in recombination reactions in the RecF pathway are discussed.\n          <\/jats:p>","DOI":"10.1128\/jb.00613-06","type":"journal-article","created":{"date-parts":[[2006,10,18]],"date-time":"2006-10-18T23:23:35Z","timestamp":1161213815000},"page":"7562-7571","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":13,"title":["<i>sbcB15<\/i>\n            and \u0394\n            <i>sbcB<\/i>\n            Mutations Activate Two Types of RecF Recombination Pathways in\n            <i>Escherichia coli<\/i>"],"prefix":"10.1128","volume":"188","author":[{"given":"Ksenija","family":"Zahradka","sequence":"first","affiliation":[{"name":"Division of Molecular Biology, Ru\u00f0er Bos\u030ckovic\u0301 Institute, Zagreb, Croatia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sanela","family":"S\u030cimic\u0301","sequence":"additional","affiliation":[{"name":"Division of Molecular Biology, Ru\u00f0er Bos\u030ckovic\u0301 Institute, Zagreb, Croatia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maja","family":"Buljubas\u030cic\u0301","sequence":"additional","affiliation":[{"name":"Division of Molecular Biology, Ru\u00f0er Bos\u030ckovic\u0301 Institute, Zagreb, Croatia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mirjana","family":"Petranovic\u0301","sequence":"additional","affiliation":[{"name":"Division of Molecular Biology, Ru\u00f0er Bos\u030ckovic\u0301 Institute, Zagreb, Croatia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Damir","family":"\u0110ermic\u0301","sequence":"additional","affiliation":[{"name":"Division of Molecular Biology, Ru\u00f0er Bos\u030ckovic\u0301 Institute, Zagreb, Croatia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Davor","family":"Zahradka","sequence":"additional","affiliation":[{"name":"Division of Molecular Biology, Ru\u00f0er Bos\u030ckovic\u0301 Institute, Zagreb, Croatia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","first-page":"5558","DOI":"10.1073\/pnas.83.15.5558","volume":"83","year":"1986","unstructured":"Amundsen, S. 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