Homolog-Dependent Repair Following Dicentric Chromosome Breakage in Drosophila melanogaster
| Autor: | Jayaram Bhandari, Travis Karg, Kent G. Golic |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
DNA Replication
Male DNA repair Mutant DNA-Directed DNA Polymerase Biology Investigations 03 medical and health sciences Dicentric chromosome 0302 clinical medicine Genetics Homologous chromosome Sister chromatids Animals Drosophila Proteins DNA Breaks Double-Stranded Mitosis 030304 developmental biology 0303 health sciences DNA Helicases Chromosome Recombinational DNA Repair Chromosome Breakage Spermatogonia Telomere Drosophila melanogaster Mutation 030217 neurology & neurosurgery |
| Zdroj: | Genetics |
| Popis: | Double-strand DNA breaks are repaired by one of several mechanisms that rejoin two broken ends. 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 δ. 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. |
| Databáze: | OpenAIRE |
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