Escape from Telomere-Driven Crisis Is DNA Ligase III Dependent
作者： Kate Liddiard , Eric A. Hendrickson , Duncan M. Baird , Rhiannon E. Jones , Sehyun Oh
DOI: 10.1016/J.CELREP.2014.07.007
关键词: Genetics 、 LIG3 、 Telomere Homeostasis 、 Dicentric chromosome 、 DNA End-Joining Repair 、 DNA ligase 、 Telomere 、 Biology 、 LIG4 、 Somatic evolution in cancer
摘要: Short dysfunctional telomeres are capable of fusion, generating dicentric chromosomes and initiating breakage-fusion-bridge cycles. Cells that escape the ensuing cellular crisis exhibit large-scale genomic rearrangements drive clonal evolution malignant progression. We demonstrate there is an absolute requirement for fully functional DNA ligase III (LIG3), but not IV (LIG4), to facilitate from a telomere-driven crisis. LIG3- LIG4-dependent alternative (A) classical (C) nonhomologous end-joining (NHEJ) pathways were mediating fusion short telomeres, both displaying characteristic patterns microhomology deletion. failed exhibited increased proportions C-NHEJ-mediated interchromosomal fusions, whereas those escaped displayed intrachromosomal fusions. propose balance between inter- telomere fusions dictates ability human cells influenced by relative activities A- C-NHEJ at telomeres.
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