{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,17]],"date-time":"2026-03-17T09:05:09Z","timestamp":1773738309799,"version":"3.50.1"},"reference-count":50,"publisher":"American Society for Microbiology","issue":"6","license":[{"start":{"date-parts":[[2004,12,1]],"date-time":"2004-12-01T00:00:00Z","timestamp":1101859200000},"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":["Eukaryot Cell"],"published-print":{"date-parts":[[2004,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Gross chromosomal rearrangements (GCRs) are frequently observed in cancer cells. Abnormalities in different DNA metabolism including DNA replication, cell cycle checkpoints, chromatin remodeling, telomere maintenance, and DNA recombination and repair cause GCRs in\n            <jats:italic>Saccharomyces cerevisiae<\/jats:italic>\n            . Recently, we used genome-wide screening to identify several genes the deletion of which increases GCRs in\n            <jats:italic>S. cerevisiae<\/jats:italic>\n            . Elg1, which was discovered during this screening, functions in DNA replication by participating in an alternative replication factor complex. Here we further characterize the GCR suppression mechanisms observed in the\n            <jats:italic>elg1<\/jats:italic>\n            \u0394 mutant strain in conjunction with the telomere maintenance role of Elg1. The\n            <jats:italic>elg1<\/jats:italic>\n            \u0394 mutation enhanced spontaneous DNA damage and resulted in GCR formation. However, DNA damage due to inactivation of Elg1 activates the intra-S checkpoints, which suppress further GCR formation. The intra-S checkpoints activated by the\n            <jats:italic>elg1<\/jats:italic>\n            \u0394 mutation also suppress GCR formation in strains defective in the DNA replication checkpoint. Lastly, the\n            <jats:italic>elg1<\/jats:italic>\n            \u0394 mutation increases telomere size independently of other previously known telomere maintenance proteins such as the telomerase inhibitor Pif1 or the telomere size regulator Rif1. The increase in telomere length caused by the\n            <jats:italic>elg1<\/jats:italic>\n            \u0394 mutation was suppressed by a defect in the DNA replication checkpoint, which suggests that DNA replication surveillance by Dpb11-Mec1\/Tel1-Dun1 also has an important role in telomere length regulation.\n          <\/jats:p>","DOI":"10.1128\/ec.3.6.1557-1566.2004","type":"journal-article","created":{"date-parts":[[2004,12,8]],"date-time":"2004-12-08T18:39:26Z","timestamp":1102531166000},"page":"1557-1566","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":39,"title":["Increased Genome Instability and Telomere Length in the\n            <i>elg1<\/i>\n            -Deficient\n            <i>Saccharomyces cerevisiae<\/i>\n            Mutant Are Regulated by S-Phase Checkpoints"],"prefix":"10.1128","volume":"3","author":[{"given":"Soma","family":"Banerjee","sequence":"first","affiliation":[{"name":"Genome Instability Section, Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kyungjae","family":"Myung","sequence":"additional","affiliation":[{"name":"Genome Instability Section, Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.286.5449.2528"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/cdg406"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1633757100"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1101\/sqb.2000.65.253"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/17.6.1819"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81175-7"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(03)00174-6"},{"key":"e_1_3_2_9_2","first-page":"81","volume":"23","year":"1999","unstructured":"Chen, C., and R. D. Kolodner. 1999. Gross chromosomal rearrangements in Saccharomyces cerevisiae replication and recombination defective mutants. Nat. Genet.23:81-85.","journal-title":"Nat. Genet."},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90105-1"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1101\/gad.14.1.81"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1101\/gad.1089203"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.2035018100"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.1006\/geno.2000.6179"},{"key":"e_1_3_2_15_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(03)00578-5"},{"key":"e_1_3_2_16_2","doi-asserted-by":"publisher","DOI":"10.1038\/8788"},{"key":"e_1_3_2_17_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1075277"},{"key":"e_1_3_2_18_2","first-page":"264","volume":"49","year":"1948","unstructured":"Lea, D. E., and C. A. Coulson. 1948. The distribution of the numbers of mutants in bacterial populations. J. Genet.49:264-285.","journal-title":"J. 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