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However, cells are challenged when asked to repair a single broken end and respond by: (1) inducing programmed cell death; (2) healing the broken end by constructing a new telomere; (3) adapting to the broken end and resuming the mitotic cycle without repair; and (4) using information from the sister chromatid or homologous chromosome to restore a normal chromosome terminus. During one form of homolog-dependent repair in yeast, termed break-induced replication (BIR), a template chromosome can be copied for hundreds of kilobases. BIR efficiency depends on Pif1 helicase and Pol32, a nonessential subunit of DNA polymerase \u03b4. To date, there is little evidence that BIR can be used for extensive chromosome repair in higher eukaryotes. We report that a dicentric chromosome broken in mitosis in the male germline of Drosophila melanogaster is usually repaired by healing, but can also be repaired in a homolog-dependent fashion, restoring at least 1.3 Mb of terminal sequence information. This mode of repair is significantly reduced in pif1 and pol32 mutants. Formally, the repaired chromosomes are recombinants. However, the absence of reciprocal recombinants and the dependence on Pif1 and Pol32 strongly support the hypothesis that BIR is the mechanism for restoration of the chromosome terminus. In contrast to yeast, pif1 mutants in Drosophila exhibit a reduced rate of chromosome healing, likely owing to fundamental differences in telomeres between these organisms.<\/jats:p>","DOI":"10.1534\/genetics.119.302247","type":"journal-article","created":{"date-parts":[[2019,5,4]],"date-time":"2019-05-04T02:05:11Z","timestamp":1556935511000},"page":"615-630","source":"Crossref","is-referenced-by-count":18,"title":["Homolog-Dependent Repair Following Dicentric Chromosome Breakage in <i>Drosophila melanogaster<\/i>"],"prefix":"10.1093","volume":"212","author":[{"given":"Jayaram","family":"Bhandari","sequence":"first","affiliation":[{"name":"School of Biological Sciences, University of Utah, Salt Lake City, Utah 84112"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Travis","family":"Karg","sequence":"additional","affiliation":[{"name":"School of Biological Sciences, University of Utah, Salt Lake City, Utah 84112"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kent G","family":"Golic","sequence":"additional","affiliation":[{"name":"School of Biological Sciences, University of Utah, Salt Lake City, Utah 84112"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2019,5,3]]},"reference":[{"key":"2022011123570317700_bib1","doi-asserted-by":"crossref","first-page":"775","DOI":"10.1093\/genetics\/148.2.775","article-title":"The transmission of fragmented chromosomes in Drosophila melanogaster.","volume":"148","author":"Ahmad","year":"1998","journal-title":"Genetics"},{"key":"2022011123570317700_bib2","doi-asserted-by":"crossref","first-page":"1041","DOI":"10.1093\/genetics\/151.3.1041","article-title":"Telomere loss in somatic cells of Drosophila causes cell cycle arrest and apoptosis.","volume":"151","author":"Ahmad","year":"1999","journal-title":"Genetics"},{"key":"2022011123570317700_bib3","doi-asserted-by":"publisher","first-page":"135","DOI":"10.1016\/j.dnarep.2018.08.017","article-title":"Preserving replication fork integrity and competence via the homologous recombination pathway.","volume":"71","author":"Ait Saada","year":"2018","journal-title":"DNA Repair (Amst.)"},{"key":"2022011123570317700_bib4","doi-asserted-by":"publisher","first-page":"13809","DOI":"10.1073\/pnas.1617110113","article-title":"Multiple mechanisms contribute to double-strand break repair at rereplication forks in Drosophila follicle cells.","volume":"113","author":"Alexander","year":"2016","journal-title":"Proc. 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