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Abstract
The Nonhomologous end joining pathway is essential for efficient repair of chromosome double strand breaks. This pathway consequently plays a key role in cellular resistance to break-inducing exogenous agents, as well as in the developmentally-programmed recombinations that are required for adaptive immunity. Chromosome breaks often have complex or “dirty” end structures that can interfere with the critical ligation step in this pathway; we review here how Nonhomologous end joining resolves such breaks.
Highlights
The non-homologous end joining pathway is essential for efficient repair of chromosome double strand breaks
Double strand break repair and complex end structures DNA double strand breaks (DSBs) arise after replication, aberrant repair of spontaneous damage, and exposure to exogenous damaging agents, especially those used in cancer therapies
Homologous recombination (HR) is dependent on extensive (100s to 1000s of nucleotides) DNA synthesis, a sister chromatid template to direct this synthesis, and a homology search step needed to find the template in a sister chromatid
Summary
The non-homologous end joining pathway is essential for efficient repair of chromosome double strand breaks. Additional factors are required, both to integrate NHEJ with the DNA damage response and local chromatin structure [7], as well as (to be discussed here) to help this core machine resolve complex ends (Table 1). NHEJ employs these additional factors according to strategies (Figure 2) for resolving complex ends we suggest can be Classes of Damage
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