Please use this identifier to cite or link to this item: https://hdl.handle.net/11147/2280
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dc.contributor.authorKoç, Ahmet-
dc.contributor.authorMerrill, Gary F.-
dc.date.accessioned2016-10-19T08:28:15Z
dc.date.available2016-10-19T08:28:15Z
dc.date.issued2007-02
dc.identifier.citationKoç, A., and Merrill, G. F. (2007). Checkpoint deficient rad53-11 yeast cannot accumulate dNTPs in response to DNA damage. Biochemical and Biophysical Research Communications, 353(2), 527-530. doi:10.1016/j.bbrc.2006.12.049en_US
dc.identifier.issn0006-291X
dc.identifier.issn0006-291X-
dc.identifier.urihttp://doi.org/10.1016/j.bbrc.2006.12.049
dc.identifier.urihttp://hdl.handle.net/11147/2280
dc.description.abstractDeoxyribonucleotide pools are maintained at levels that support efficient and yet accurate DNA replication and repair. Rad53 is part of a protein kinase regulatory cascade that, conceptually, promotes dNTP accumulation in four ways: (1) it activates the transcription of ribonucleotide reductase subunits by inhibiting the Crt1 repressor; (2) it plays a role in relocalization of ribonucleotide reductase subunits RNR2 and RNR4 from nucleus to cytoplasm; (3) it antagonizes the action of Sml1, a protein that binds and inhibits ribonucleotide reductase; and (4) it blocks cell-cycle progression in response to DNA damage, thus preventing dNTP consumption through replication forks. Although several lines of evidence support the above modes of Rad53 action, an effect of a rad53 mutation on dNTP levels has not been directly demonstrated. In fact, in a previous study, a rad53-11 mutation did not result in lower dNTP levels in asynchronous cells or in synchronized cells that entered the S-phase in the presence of the RNR inhibitor hydroxyurea. These anomalies prompted us to investigate whether the rad53-11 mutation affected dNTP levels in cells exposed to a DNA-damaging dose of ethylmethyl sulfonate (EMS). Although dNTP levels increased by 2- to 3-fold in EMS treated wild-type cells, rad53-11 cells showed no such change. Thus, the results indicate that Rad53 checkpoint function is not required for dNTP pool maintenance in normally growing cells, but is required for dNTP pool expansion in cells exposed to DNA-damaging agents.en_US
dc.language.isoenen_US
dc.publisherElsevier Ltd.en_US
dc.relation.ispartofBiochemical and Biophysical Research Communicationsen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectDNA damageen_US
dc.subjectdNTPen_US
dc.subjectEMSen_US
dc.subjectRad53en_US
dc.subjectYeasten_US
dc.titleCheckpoint deficient rad53-11 yeast cannot accumulate dNTPs in response to DNA damageen_US
dc.typeArticleen_US
dc.authoridTR110769en_US
dc.institutionauthorKoç, Ahmet-
dc.departmentİzmir Institute of Technology. Molecular Biology and Geneticsen_US
dc.identifier.volume353en_US
dc.identifier.issue2en_US
dc.identifier.startpage527en_US
dc.identifier.endpage530en_US
dc.identifier.wosWOS:000243543100049en_US
dc.identifier.scopus2-s2.0-33845761546en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.identifier.doi10.1016/j.bbrc.2006.12.049-
dc.identifier.pmid17188244en_US
dc.relation.doi10.1016/j.bbrc.2006.12.049en_US
dc.coverage.doi10.1016/j.bbrc.2006.12.049en_US
local.message.claim2022-06-06T11:53:20.650+0300|||rp00417|||submit_approve|||dc_contributor_author|||None*
dc.identifier.wosqualityQ2-
dc.identifier.scopusqualityQ1-
item.openairetypeArticle-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextWith Fulltext-
item.languageiso639-1en-
item.cerifentitytypePublications-
item.grantfulltextopen-
crisitem.author.dept04.03. Department of Molecular Biology and Genetics-
Appears in Collections:Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik
PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection
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