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. 2015 Aug 15;6(3):110–134. doi: 10.1159/000438812

Table 1.

Mechanisms of CCR formation, involved genes and molecular signatures of joining points

FoSTeS MMBIR Breakage-fusion-bridge cycle Chromothripsis
Causes stalled replication forks DSBs ? overactivity of SPO11, free radicals or ionizing radiation, covalent DNA damage interfering with resolution of Holliday junctions or defective cell cycle checkpoints

Basic mechanism strand invasion by lagging DNA replication strand joining of 2 open DNA strands ? NHEJ and MMBIR

Enzymatic activities DNA replication machinery exonuclease-mediated resection artemis-nuclease, gap-filling DNA polymerase, ligase 4 not studied

Associated CNVs deletions, duplications, triplications none none only losses, no duplications; pachytene stage of meiosis I

DNA fragment orientation head-to-tail head-to-tail head-to-tail randomly joined in head-to-tail, tail-to-tail and head-to-head orientations

Junction sequences ? microhomologies, short deletions, non-templated insertions small deletions due to NHEJ losses of a few base pairs up to several kb, small insertions of non-templated sequences

Junction spacing ? ? ? closely spaced

Key references Hastings et al., 2009; Colnaghi et al., 2011 Hastings et al., 2009; Colnaghi et al., 2011 Scott and Pandita, 2006 Liang et al., 1998; Holloway et al., 2010; Truong et al., 2013

? = Not known.